
Glass 
Book 



COPYRIGHT DEPOSIT 



I 



"With all our varied instruments of precision, useful as they 
are, nothing can replace the watchful eye, the alert ear, the tactful 
finger, and the logical mind which correlates the facts obtained 
through all these avenues of information and so reaches an exact 
diagnosis. " 

W. W. KEEN. 






PRINCIPLES AND PRACTICE 



OF 



PHYSICAL DIAGNOSIS 



BY 

JOHN C DaCOSTA, Jr., M. D. 

EX-ASSOCIATE PROFESSOR OP MEDICINE, JEFFERSON MEDICAL COLLEGE AND ASSISTANT 
VISITING PHYSICIAN, JEFFERSON HOSPITAL; CONSULTING PHYSICIAN, NORTHWESTERN 
GENERAL HOSPITAL; FELLOW OF THE COLLEGE OF PHYSICIANS OF PHILADEL- 
PHIA; FELLOW OF THE AMERICAN ACADEMY OF MEDICINE; MEMBER 
OF THE AMERICAN THERAPEUTIC SOCIETY, ETC. 



FOURTH EDITION, THOROUGHLY REVISED 



PHILADELPHIA AND LONDON 

W. B. SAUNDERS COMPANY 

1919 



mi 



Copyright, 1908, by W. B. Saunders Company. Reprinted June, 1909, and 
September, 1910. Revised, reprinted, and recopyrighted September, 
191 1. Reprinted August, 1913. Revised, reprinted, and recopy- 
righted November, 191 5. Revised, reprinted, and recopy- 
righted November, 191 9 



Copyright, 1919, by W. B. Saunders Company 



NOV 14 1919 



PRINTED IN AMERICI 



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TO THE MEMORY OF 
MY UNCLE 

JOHN MEIGS, Ph. D. 

HEAD MASTER OF THE HILL SCHOOL 



PREFACE TO THE FOURTH EDITION 



The new matter in this edition chiefly concerns the lungs and 
the heart, gas edema, gas pneumonia, influenzal pneumonia, and 
hilus tuberculosis being included under the former heading; and 
the effort syndrome, the functional capacity of the heart, aviator's 
heart, and sino-auricular block under the latter caption. The 
clinical relations and physical signs of cecum mobile are dealt with 
in detail. Improvements in various technical methods of physical 
examination have been described from the clinician's viewpoint, 
notably those relating to sphygmomanometry, to intradural pres- 
sure, and to the estimation of the cardiac reserve force. 

Aside from the foregoing more important additions, the entire 
text of the last edition has been critically revised and several new 
illustrations have been added, without change in the original 
character and scope of the previous printings, and with but mod- 
erate increase in the size of the book. 

Philadelphia, November, 1919. 



- 



PREFACE 



The purpose of this book is to present, within reasonable compass, 
the principles of physical diagnosis, and to apply this means of 
research to the study of thoracic and abdominal diseases. To meet 
the requirements of junior students, especial consideration is given 
to clinical anatomy and to the origin, mechanism, and meaning of 
normal physical signs; while in order to guide those farther advanced 
in the study and practice of medicine, the subjects of pathology and 
diagnosis are accorded commensurate prominence. Throughout, 
a consistent endeavor is made to keep in view the prime impor- 
tance of interpreting morbid objective data, individual or grouped, 
on the basis of pathologic cause and physical effect, and to analyze 
such findings in the light of a full clinical inquiry. In the section 
dealing with technic the theory and practice of the simpler direct 
methods of physical examination are explained in detail, and also 
certain instrumental procedures adapted to routine bedside inves- 
tigation. Useful laboratory information, in so far as it applies to 
the diagnosis of particular lesions, is discussed in connection there- 
with, but an account of special laboratory technic, not being germane 
to the plan of this work, is omitted. 

The subject matter of the following pages is based primarily upon 
the author's lecture-notes, and the' views expressed were molded 
largely by ten years' clinical and teaching experience in internal 
medicine and study of pathology, aided and supplemented by much 
information derived from acknowledged authorities and from con- 
tributions of merit found in text-books, monographs, and periodical 
literature. Information gleaned from these sources has been duly 
accredited in the text, save in the case of facts that by time and usage 
have become a matter of common scientific knowledge. 

5 



6 PREFACE 

Care has been taken to secure an adequate number of original 
illustrations that will prove helpful to the reader, those representing 
various clinical conditions having been reproduced from photographs 
of patients observed in the Jefferson Hospital and in the Philadelphia 
General Hospital, and those showing pathologic lesions having been 
made from Kaiserling preparations by Dr. R. C. Rosenberger and 
Dr. John Funke, of the pathological staffs of these institutions. 
Recknagel model-studies and figures standardized to Cunningham 
have been utilized for many of the diagrams by Mr. E. F. Faber 
and by Mr. J. V. Alteneder. The sphygmograms and cardiograms 
are the work of Dr. George Bachmann, and the radiographic plates 
were made by Dr. W. F. Manges. For the cooperation so cordially 
extended by these gentlemen hearty thanks are herewith returned. 

The author takes pleasure in acknowledging the aid rendered 
by his wife in lightening the task of proof-revision; in thanking 
Dr. S. A. Munford for many useful criticisms and suggestions 
relating to technical questions; and in expressing appreciation of 
his publishers' numerous courtesies and liberal policies. 



CONTENTS 



SECTION I 

Page 

Methods and Technic of Physical Examination n 

Inspection 12 

Palpation 12 

Percussion 12 

Auscultation 22 

Thoracometry and Cyrtometry 29 

Sphygmomanometry 31 

Sphygmography and Cardiography 37 

Electrocardiography 44 

Paracentesis 47 

Fluoroscopy and Radiography 67 

The Tuberculin Reaction 68 

SECTION Ii 

Examination of the Thorax 72 

Clinical Anatomy 72 

Normal Landmarks 73 

Topographic Lines and Areas 76 

Pathologic Types 79 

Local Asymmetry 88 

Respiratory Movements 94 

Anomalies of Respiration 97 

Dyspnea 102 

Cyanosis 106 

Venous Enlargement and Tortuosity 106 

Edema of the Thoracic Wall 108 

Glandular Enlargement in 

Pain in the Thorax 119 

SECTION III 

Examination of the Bronchopulmonary System I2 4 

Clinical Anatomy 1 24 

Inspection 130 

Palpation 132 

Percussion 138 

Auscultation of the Lungs 155 

Respiratory Sounds 156 

Vocal Resonance 163 

Adventitious Sounds 164 

Splashing Sounds 173 

7 



8 CONTENTS 

SECTION IV Page 

Diseases of the Bronchopulmonary System and Mediastinum 175 

Acute Catarrhal Bronchitis 175 

Chronic Catarrhal Bronchitis 178 

Fibrinous Bronchitis 179 

Bronchial Asthma 181 

Bronchiectasis • 183 

Bronchostenosis 187 

Pulmonary Congestion 189 

Pulmonary Edema 192 

Pulmonary Hemorrhagic Infarction 195 

Catarrhal Pneumonia 197 

Croupous Pneumonia 203 

Chronic Interstitial Pneumonia 219 

Acute Pneumonic Phthisis 222 

Chronic Ulcerative Phthisis 226 

Fibroid Phthisis 241 

Pulmonary Syphilis 244 

Emphysema 247- 

Hypertrophic '. 248 

Atrophic 253 

Compensatory 253 

Acute Vesicular 254 

Interstitial 255 

Atelectasis 255 

Pneumonoconiosis 259 

Pulmonary Abscess 262 

Pulmonary Gangrene 264 

Pulmonary Neoplasms 267 

Actinomycosis 271 

Echinococcus Cyst 272 

Pleurisy. 273 

Acute Fibrinous 274 

Serofibrinous 275 

Purulent 285 

Circumscribed 288 

Chronic Adhesive 290 

Hydrothorax 292 

Hemothorax 293 

Chylothorax 294 

Pneumothorax 294 

Pleural Neoplasms 302 

Mediastinitis 303 

Mediastinal Lymphadenitis 306 

Mediastinal Neoplasms 309 

SECTION V 

Examination of the Cardiovascular System 316 

Clinical Anatomy 316 

Mechanism of the Circulation 319 

Inspection and Palpation 323 

Percussion 358 

Auscultation 363 

Adventitious Sounds 380 

Endocardial Murmurs 381 

Exocardial Sounds 397 

Vascular Murmurs 400 

Functional Capacity of the Heart 403 



CONTENTS 9 

SECTION VI Page 

Diseases of the Cardiovascular System 405 

Pericarditis 405 

Soldier's Heart * 405 

Acute Fibrinous 408 

Serofibrinous ^ 1Q 

Purulent 4'^ 

Chronic Adhesive 4™ 

Jiydropericardium 4^ 

Hemopericardium , ^ I g 

Pneumopericardium 4x8 

Cardiac Hypertrophy 4jg 

Cardiac Dilatation 425 

Myocarditis 429 

Acute Endocarditis 433 

Chronic Endocarditis 439 

Mitral Regurgitation 446 

Mitral Stenosis 45I 

Aortic Regurgitation 46! 

Aortic Stenosis 469 

Tricuspid Regurgitation 474 

Tricuspid Stenosis 477 

Pulmonary Stenosis 479 

Pulmonary Regurgitation 483 

Congenital Cardiac Disease 485 

Aneurism of the Aorta '. 488 

Aneurism of Thoracic Aorta 488 

Aneurism of Abdominal Aorta 505 

SECTION VII 

Examination of the Abdomen and the Abdominal Viscera 507 

Clinical Anatomy 507 

Topographic Lines and Areas 510 

Methods of Abdominal Examination 512 

Clinical Types of Abdomen 515 

Local Abdominal Enlargements 521 

Abdominal Movements 524 

The Skin and Subcutaneous Tissues 525 

Fluctuation 527 

Tactile Friction and Thrills 528 

Pain in the Abdomen 528 

Examination of the Stomach 531 

Examination of the Intestines 544 

Examination of the Liver and Gall-bladder 552. 

Examination of the Pancreas 562 

Examination of the Spleen 563 

Examination of the Kidneys 570 

lNDEX 575 



Physical Diagnosis 



SECTION I 



METHODS AND TECHNIC OF PHYSICAL 
EXAMINATION 



In the common acceptance of the term, physical diagnosis relates 
primarily to the objective study of disease by the four cardinal methods 
of inspection, palpation, percussion, and auscultation, the success- 
ful practice of which depends upon the intelligent exercise of the 
examiner's senses of sight, feeling, and hearing. In suitable instances 
certain clinical instruments are used as an aid and a supplement to 
these means of inquiry: the thermometer, to take the patient's tem- 
perature; the stethoscope, to facilitate auscultatiou; the tape-measure, 
calipers, and cyrtometer, to determine diameters, circumferences, 
and shapes; the exploring needle, to obtain specimens of body-fluids; 
and the tonometer, the sphygmograph, and the electrocardio- 
graph, to study the blood-pressure and other details of the 
circulatory system. 

In addition to the foregoing methods of physical diagnosis the 
clinician has at his disposal a number of technical procedures that 
require training in the use of special instruments of precision and in 
laboratory technic, and upon the intimate correlation of the data 
derived from both these sources, bedside and laboratory, a finished 
diagnosis must be based. Although, in a broad sense, the diagnostic 
application of the Rontgen-ray and analyses of the urine, blood, 
sputum, gastro-intestinal contents, and body-fluids belong to the 
subject of physical diagnosis, the technic and principles of these pro- 
cedures are too highly specialized to receive more than parenthetic 
reference in the following pages, which deal purely with the theory 
and practice of physical diagnosis at the bedside, with reference to 
the study of thoracic and abdominal lesions. 



12 PHYSICAL DIAGNOSIS 

INSPECTION 

Inspection, or visual examination of the patient, is the first, and in 
some instances the all-important, step in a routine physical examina- 
tion. "We make more mistakes by not looking than by not know- 
ing" is an aphorism of Edward Jenner that every beginner in tre 
study of physical diagnosis should take as a maxim. To neglect 
or to gloss over careful inspection of the patient deprives one of a 
means of information for which skill in percussion or in ausculta- 
tion cannot compensate. 

A general inspection shows the individual's appearance, body con- 
formation, and gait; the approximate height and weight; the con- 
dition of the muscular and adipose structures; and the marks of 
various cachexias and of scarring or eruptive diseases. Inspection 
of a circumscribed area, with the patient's clothing removed, may 
betray at a glance some organic lesion, or at least may give a clue 
to be verified by other procedures. The facies of pneumonia, of 
phthisis, and of Bright's disease, the barrel chest of emphysema, 
and the throbbing tumor of aneurism are familiar examples of dis- 
eases that in time indelibly stamp their subjects with visible signs 
so characteristic as immediately to direct the clinician along cor- 
rect fines of inquiry. 

PALPATION 

Palpation, or examination by means of the tactile sense of the fingers 
and the palms of the hands, is employed in studying various vibrations 
referable to the bronchopulmonary system (fremitus) , to the cardio- 
vascular apparatus (thrill), and to the serous surfaces (friction). 
The palpating hand can also appreciate the wavy impulse of pent-up 
fluid agitated by striking its delimiting parietes (fluctuation), and 
can recognize rhythmic throbbing of cardiovascular origin (pulsa- 
tion). The site, size, shape, mobility, resistance, and tenderness of 
a local area of the body are also determined principally by the tactile 
sense of the examiner's hand. 

The special technic of inspection and palpation in the examina- 
tion of various regions and organs is described subsequently. 

PERCUSSION 

Percussion is the act of striking or tapping the surface of the 
body so as to elicit sounds of diagnostic utility, the clinical value 
of this method depending upon the fact that different anatomic 
structures, when struck by the finger-tips or with a suitable instru- 
ment, give rise to different sounds, the acoustics of which vary accord- 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 1 3 

ing to the physical properties of the parts percussed. Fundamen- 
tally, all percussion-sounds are either resonant or dull, of which 
essential properties there are several modifications, notably, hyper- 
resonance, tympany, and flatness, together with several other special 
shades of sound not exactly expressed by any of these terms. By 
noting the character of the sounds and the degree of resistance over 
the region percussed, one is able to judge the density of the under- 
lying structures and to delimit the 
boundaries of parts containing dif- 
ferent volumes of air. 

The percussion blow may be 
struck either with the finger-tips 
(finger percussion) or with a small 
hammer (instrumental percussion). 
By the method known as mediate 
percussion the sound is elicited by 
laying a finger (pleximeter finger) 
flat upon the part and tapping it 
with one or two fingers (plexor fin- 
gers) of the other hand; or a small 
rubber plate may be used as a 
pleximeter and a specially devised 
percussion hammer as a plexor. 
In the practice of immediate per- 
cussion, little used at the present 
time, the part is tapped without the Fig. 1 — Technic of mediate percus- 
intermediation of a pleximeter. 

Percussion, though exploited by Auenbrugger ;n 1761, did not 
come into general use until half a century later, when, in 1808, 
Corvisart's researches, prompted largely by the teachings of Stoll, 
crystallized the diverse and fantastic theories and methods of per- 
cussion into a tangible, concrete means of clinical inquiry. Piorry 
and Barry, the advocates of instrumental percussion, and Skoda, 
who, in 1839, correlated the various percussion-sounds with correct 
physical factors, were conspicuous figures in the development of 
Auenbrugger's principle, now so indispensable to diagnosis. 

Technic. — It is best to percuss the bare surface of the body, though 
a thin covering of underclothing does not materially interfere. Mus- 
cular relaxation, natural breathing, and an unconstrained posture, 
either erect or prone, as the circumstances direct, are requisites for 
the best results. 

In performing mediate finger percussion (Fig. i) the palmar 




14 PHYSICAL DIAGNOSIS 

surface of the middle finger of the left hand is laid upon the surface 
of the body and sharply struck with the tip of the middle finger of 
the right hand, the plexor finger being crooked so as to deliver a per- 
pendicular blow, which should fall upon the dorsal surface of the 
pleximeter finger at the base of the nail or at the middle of the second 
phalanx. Four precautions are to be observed: the pleximeter finger 
must be kept in firm, close, accurate contact with the surface of the 
body; the force of the percussion strokes must be as equal as possi- 
ble; the blow must be delivered entirely by a movement of the wrist, 
with the elbow rigid and immovable; and the action of the plexor 
finger must be rapid, accurate, and rebounding. The force of the 
stroke is strong or light, according to the situation of the organ or 
lesion percussed, whether deep or superficial. (See Fig. 77.) Too 
forcible percussion, even of a deep-seated structure, is to be guarded 
against, since it may set up such intense vibrations outside of the 
circumscribed area that a confusing commingling of sounds is pro- 
duced. The more forcible the percussion-stroke, the firmer should 
be the pressure of the pleximeter finger, and vice versa. The plexi- 
meter finger should be kept parallel to the outline of the part to 
be delimited. A few careful strokes will demonstrate the character- 
istics of the sounds and of the resistance much better than a long 
succession of blows. Prolonged percussion dulls one's auditory and 
tactile perceptions, just as long-continued looking at the two tints in 
a hemoglobinometer blunts one's color-sense. 

Goldscheider's method of threshold percussion may prove use- 
ful in outlining the cardiac and hepatic borders, the technic con- 
sisting of tapping lightly with the finger upon a glass rod pleximeter 
one end of which, fitted with a rubber cap, rests upon an intercostal 
space, the rod meanwhile being held at an angle to the surface of the 
thorax and parallel to the borders of the organ thus to be delimited. 
This method of percussion possesses the advantage of confining the 
percussion vibrations to a very restricted area, and affords accurate 
data at the hands of one skilled in its use. 

Immediate percussion is performed by directly striking the sur- 
face with a plexor (finger or instrumental), or of delivering a series 
of sharp slaps with the flat of the hand. The method is distinctly 
inferior to mediate percussion, owing to the defective sounds pro- 
duced and also because it robs the examiner of definite tactile impres- 
sions, so essential in judging the character of sounds. Immediate 
percussion is employed chiefly in demonstrating extensive areas of 
dulness and tympany, in eliciting the cardiac and the pulmonary 
reflexes, and in the practice of auscultatory percussion (q. v. i.). 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 



15 



Palpatory percussion is a combination of palpation and percus- 
sion affording tactile rather than auditory impressions, which are 
elicited by gently striking the pleximeter finger with the pads of the 
plexor fingers, the latter being kept almost straight, so as to produce 
more of a pushing impact than a perpendicular blow, this peculiarity 
being the more emphasized by continuing the plexor-pleximeter 
pressure for a few moments after the stroke. Rebounding piano- 
hammer strokes are to be avoided, and the arc of the percussion 
push should not exceed one or two inches (2.5 to 5 cm.). 
Although perhaps a superior method of examination for those 




Fig. 2. — Technic of auscultatory percussion. 

skilled in its technic, palpatory percussion is in no sense a substi- 
tute for ordinary mediate percussion in routine work. 

Auscultatory Percussion. — Auscultatory or stethoscopic per- 
cussion is the act of listening to the percussion-sounds with a stetho- 
scope applied to the part under examination, instead of directly 
judging the sound in the ordinary manner. It is adapted especially 
to outlining various solid and hollow organs, such as the heart, the 
liver, the spleen, the stomach, and the colon; in determining the 
limits of effusions and consolidations; and in circumscribing cavities 
and tumors. By auscultatory percussion of a superficial echinococ- 
cus cyst it is sometimes possible to distinguish a deep, sonorous 
sound of hydatid resonance. 



i6 



PHYSICAL DIAGNOSIS 



In auscultatory percussion the chest-piece of a binaural stetho- 
scope is placed over the part to be delimited, 1 where it is held in 
position by the patient or by an assistant, while the examiner, listening 
through the instrument, begins to percuss very gently at several 
points encircling the organ and well beyond its outer boundary 
(Fig. 2). Continuing the percussion toward the organ, along con- 
verging lines centering at the chest-piece of the stethoscope, the 
sounds become distinctly louder and altered in pitch and in quality 
when the periphery of the organ is reached. A line joining these 




am >- 



■bf-l — > © < \\b - 



+a 




Fig. 3. — Illustrating the technic of auscultatory percussion: a-b, Percussion lines; 
b, points of acoustic change; c, chest-piece of stethoscope. 



several points of acoustic change corresponds to the limits of the 
organ in question (Fig. 3). 

Several modifications of this, the usual, technic of auscultatory 
percussion also enjoy more or less vogue, and perhaps merit con- 
fidence. Thus, the sound may be produced by direct stroking of 
the surface with the finger-tips, instead of by actual percussion — 
stroke auscultation; by rubbing the fingers up and down, a grooved 
wooden stick applied perpendicularly to the surface — rod ausculta- 
tion (Reichmann) ; or by tapping with one forefinger the second 

1 Le Fevre prefers to auscultate the percussion-sounds with the chest-piece of 
the stethoscope held just above the point of percussion, but not touching the 
surface, in order to eliminate the vibrations of the bony thorax. 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 1 7 

joint of the other forefinger applied perpendicularly to the part — 
KordnyVs method. The substitution of a vibrating tuning-fork for 
the plexor finger has been suggested (Warder), the examiner noting 
the changes in the intensity and quality of the musical vibrations as 
the fork passes over the surface toward the part under investi- 
gation. 

Attributes of the Percussion-sound. — Four different acoustic 
properties, quality, pitch, duration, and intensity, are to be recognized 
as clinically important attributes of the percussion-sound. Since 
verbal description can convey but an inadequate idea of these funda- 
mental sound elements, each one must be studied practically by the 
student in order to appreciate their individual peculiarities. Their 
every-day application will be understood when they are referred to 
later, in connection with the questions of resonance, dulness, and 
other phases of the percussion-sound. The resistance offered to the 
plexi meter (or percussed) finger is also of the greatest utility in deter- 
mining the nature of the region examined. 

By the term quality is meant that essential element by which the 
particular source of a given sound is distinguished, whether it be a 
vocal, an instrumental, or other tone. Thus, this quality, timber, or 
tone-color enables one instantly to discriminate between a masculine 
and a feminine voice, between the sounds of a bass-drum and a snare- 
drum, and between the tones of a fife and an oboe, a piano and an 
organ, and other musical instruments. Physically, the quality of 
sounds is determined by the type of vibrations by which they are 
generated, the more complex vibrations giving rise to sounds of greater 
individuality than those of simpler character. It is this element of 
quality, then, that is the clue to the origin and nature of different 
sounds, which cannot be judged by criteria such as pitch, intensity, 
and duration. 

The pitch of a sound is an acoustic attribute thoroughly appreci- 
able only by those who are gifted with a "musical ear." It was 
Austin Flint who first called attention, in 1852, to the value of 
pitch variations in the acoustics of percussion and respiratory 
sounds. Variations in pitch are governed by the rate of the vibra- 
tions set up in the part percussed, and the more rapidly these vibra- 
tions occur, the higher the pitch, and vice versa. The deep rumble 
of the basso and the high "A" of the soprano exemplify extremes of 
low and of high pitch respectively, while by their quality the sounds 
are recognized as the male and the female human voices. Other con- 
ditions being the same, a tense muscular thorax yields a percussion 
sound of higher pitch than a relaxed, thin chest, and the same is true 



1 8 PHYSICAL DIAGNOSIS 

of a small thorax in comparison with a large one. Similarly, higher 
pitched sounds are afforded by small than by large air-containing 
viscera, cavities, and consolidations, by muscle than by lung, and 
by pleural effusion than by pulmonary infiltration. 

The duration of a sound, which is an element of subsidiary impor- 
tance, expresses simply its length or continuance. Duration and 
pitch are intimately related, in that the lower the pitch, the longer 
the duration, and vice versa. For instance, normal low-pitched 
pulmonary resonance is of longer duration than the sound obtained 
by percussing over a high-pitched patch of pneumonic or tuberculous 
consolidation. 

Intensity, or volume, also of secondary importance, refers to the 
degree of fulness, loudness, or amplitude of a sound. It goes hand 
in hand with the foregoing attributes, pitch and duration, especially 
with the latter — the longer the duration of a sound, the greater its 
intensity. Thus, normal pulmonary resonance yields a more intense 
sound than a consolidated area, while, on the other hand, the sound 
over a small cavity is feebler than that over an extensive excavation. 
The intensity of a sound is determined by several factors, of which 
the most important are the force of the percussion stroke, the amount 
of air contained in the part percussed, and the thickness and resiliency 
of the intervening structures. 

Sense of Resistance. — The resistance appreciated by the plexi- 
meter finger when the percussion blow is delivered is, to the experi- 
enced clinician, quite as certain a guide as the actual sound elicited. 
This resistance is a particularly useful clue in ill-defined pulmo- 
nary consolidations in which exaggerated fremitus, frank dulness, 
and definite auscultatory signs are wanting, and in such instances 
a high-pitched sound with an increased feeling of resistance is 
often conclusive evidence. Percussion of the thigh gives a good 
example of greatly increased resistance, and over the colon, an 
illustration of diminished resistance. The resistance is strikingly 
exaggerated over a pleural effusion, well marked over a consoli- 
dated lung, and usually diminished over a pneumothorax. As a 
general rule, it may be stated that tactile resistance increases pari 
passu with the extent to which the air contained in an organ is replaced 
by liquid or solid matter, and with the increase in the tension of the 
parietal structures. 

Tonal Properties of the Percussion-sound. — Resonance. — If an 
air-containing organ, such as the lung, be percussed, the sound elicited 
has a clear, soft, resounding quality, a moderately low pitch, and a 
well-sustained duration and intensity. This typically resonant sound, 
or pulmonary resonance, though pure and clear, lacks the harmony 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 1 9 

and consonance of a true musical note, for it is caused by the vibra- 
tions of air-columns, which, owing to the peculiarities of the broncho- 
pulmonary structures, lack precise rhythm and equality of sound- 
waves. 

Tympany. — If an air-containing organ, such as the stomach, be 
percussed, a clear, hollow sound is produced, differing chiefly from 
pulmonary resonance in having a distinctive drum-like quality. This 
tympanitic resonance, or tympany, is a typical musical note, since it 
is due to rhythmic vibrations of sound-waves of equal length occur- 
ring within an empty cavity bounded by thin, smooth, elastic walls. 

Hyperresonance. — Percussion of an overdistended lung, as in 
hypertrophic emphysema, creates a sound which, though it retains the 
quality of normal pulmonary resonance, differs from it in possessing 
greater intensity and lower pitch. Such a sound approaches tym- 
pany, yet it cannot be so designated, because it lacks the true tym- 
panitic or drum-like quality. The compromise term, hyperresonance, 
is, therefore, applied to this tone, used to signify the various shades 
of exaggerated resonance not amounting to actual tympany. 

Independent of the above-mentioned physical causes is the sound 
elicited by percussion over a bony structure, which, when struck, 
vibrates resonantly by virtue of its inherent resiliency, and emits a 
sound termed osteal resonance. The qualities of the osteal tone are 
well illustrated by percussion over the sternum. Auscultatory per- 
cussion over an echinococcus cyst yields a peculiar low-pitched sonor- 
ous tone, known as hydatid resonance; provided that the cyst is super- 
ficial, and contains a thin liquid inclosed within resilient walls. This 
sound is due to the same factors responsible for hydatid fremitus 
(q. v.) , of which it is the tonal equivalent. 

Certain forms of modified resonance — amphoric, cracked-pot, and 
vesiculotympanitic — are discussed in connection with the special 
circumstances under which they occur. (See p. 150 et seq.) 

Dulness and Flatness. — These two words express varying degrees 
of impaired resonance, ranging from the trifling impurity of sound 
due to a slight diminution of air in a part, to the absolute deadness 
found over an entirely airless structure. Flatness is the acoustic 
acme of dulness, and between the two extremes numerous tonal 
gradations exist, designated, for convenience sake, as impaired reso- 
nance and relative dulness. 

The terms dulness and flatness are not to be used synonymously: 
the former is applied to a sound which, though impaired, still retains 
some element of resonance, and the latter to a sound to which even 
the faintest trace of resonance is foreign. A dull sound indicates 
that the air-content of the part within range of percussion is dimin- 



2 o PHYSICAL DIAGNOSIS 

ished, but not absolutely abolished, the latter condition being betrayed 
by flatness. For example, the percussion-sound over a patch of 
pneumonic hepatization is dull, not flat, inasmuch as the consolidated 
lung is not entirely deprived of air, owing to the fact that the com- 
municating bronchi and many groups of unimplicated vesicles con- 
tain a sufficient volume of air to emit a feeble shade of resonance. 
On the other hand, a pleural effusion, being quite airless, affords pure 
flatness without a suspicion of resonance. 

According to their acoustic attributes, it will be noted that, as the 
dull percussion-sound approaches flatness, the quality hardens, the 
pitch rises, the intensity and duration diminish, and the resistance 
increases. A slight elevation in pitch plus increase in the resistance 
over the part percussed is one of the earliest signs of impaired reso- 
nance, and, since it is usually appreciable before the development 
of frank dulness, the finding is most pertinent. 

The resonant quality of an air-containing part is materially modi- 
fied by the degree of tension existing in its walls, which, to resound 
resonantly, must be sufficiently relaxed to vibrate freely under the 
impact of the percussion blow. Up to a certain point of mural ten- 
sion the sound remains clear, but if the tension be raised beyond 
this "resonant point," the purity of the sound disappears and it 
becomes dulled and toneless. In a similar manner undue lowering 
of the mural tension dulls a resonant sound. 

The pitch of resonance varies according to the volume of air con- 
tained in the part emitting the sound : the pitch of pulmonary reso- 
nance, for example, rises as the air-content of the lung is lessened by 
the encroachment of a consolidation, as in croupous pneumonia; 
the pitch of the note is higher over the small intestine than over the 
large gut. 

The intensity and the duration of resonance are determined by 
the force and the length of the sound-waves within the part per- 
cussed: other conditions being equal, the larger the air-space within 
the organ, the louder and the more lasting the sound evoked by per- 
cussion. 

Aside from the influences of mural tension and air- volume in modify- 
ing the resonance of an air-containing part, the force of the percus- 
sion blow and the vibratory properties of the tissues within its range 
are also determining factors of the sound produced. 

Spinal Percussion. — Spinal percussion is not without value in 
the study of obscure lesions of the lungs and mediastinum lying 
close enough to the spine to damp its vibrations, but too far from the 
thoracic wall to produce definite dulness thereupon. Healthy verte- 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 21 

brae emit osteal percussion-sounds sui generis in quality, and of a 
degree of resonance corresponding to the extent to which the bone 
vibrations are affected by adjacent anatomic structures. The accom- 
panying diagram (Fig. 4) shows a clinical modification of Koranyi's 
spinal zones, each affording, in health, distinctive percussion find- 
ings which are variously altered by morbid processes of the thorax 
and abdomen. Thus, the normal dulness of the uppermost zone 
diminishes vertically in hypertrophic emphysema, but lengthens in 




L- IV. thoracic 
(dulness) 



> V.-XII. thoracic 
(osteal resonance) 



I Lumbar (impaired 
resonance) 



I Sacral (flat tympany) 



Fig. 4. — Spinal percussion zones. 



mediastinal neoplasm and in thoracic aneurism. Pulmonary con- 
solidation may appreciably dull the osteal resonance of the thoracic 
zone, while fluid within the pleural sac causes dulness at the base of 
this region and extending thence upward to a height commensurate 
with the volume of the effusion. (See Grocco's Triangle, p. 280.) 
A tumor of the abdomen (i. e., hepatic, splenic, or pancreatic) may 
substitute absolute dulness for the normal impaired resonance of the 
lumbar zone and even obliterate the flat tympany below. Spinal per- 
cussion is usually performed with the aid of a soft-rubber plexor and 



2 2 PHYSICAL DIAGNOSIS 

vulcanite pleximeter, the latter being placed over the spinous proc- 
esses, but the writer prefers to use ordinary mediate ringer percus- 
sion in order to judge tactile resistance as well as tonal changes. 

By percussion of the vertebral tips and the upper interscapular 
region Ewart has mapped out a paravertebral ovoid subresonant 
area between the first and the fifth thoracic spines, extending 
vertically for no mm. and having an equatorial diameter of 90 mm., 
each lateral boundary being equidistant from the midline. This 
ovoid patch contracts laterally with deep inspiration and com- 
mensurately expands with expiration. In apical phthisis and 
pleurisy its respiratory excursions are restricted and its sym- 
metry is altered, and in hypertrophic emphysema, in addition, 
the size of the patch is greatly diminished. Extension of dul- 
ness in this region, with modification of the normal ovoid shape, 
has been reported in tracheobronchial adenopathies, in peri- 
cardial effusion, in extensive enlargement of the left auricle, in 
aortic aneurysm, and in enlarged thymus. 

Vertebral reflexes (Abrams) are demonstrable by the percussion 
of appropriate spinous processes, whereby contraction and dilatation 
of the deep viscera are provoked if the organs in question be healthy. 
Upon this fact depends the clinical utility of the test, which consists 
of outlining the organ, by topographic percussion, both before and 
after vertebral concussion, and of comparing the size of the two 
boundaries. In health, percussion of the lower five thoracic spines 
should enlarge, and of the vertebra prominens should diminish, the 
cardiac and aortic areas of dulness anteriorly, while percussion of the 
upper three lumbar vertebrae should reflexly contract the normal 
areas of the liver, the spleen, and the stomach. Spinal reflexes are 
usually evoked by delivering a few sharp blows with a plexor upon the 
spinous processes, the outline of the organ before and after this 
manoeuver being judged by auscultatory percussion. 

AUSCULTATION 

Auscultation, as applied to clinical examinations, is the act 
of listening to physical sounds, normal and pathologic, either by 
the aid of an instrument known as a stethoscope, or by applying 
the ear directly to the part. This method of research is employed 
chiefly in investigating the condition of the respiratory system 
and the heart, but in certain instances it gives useful data relat- 
ing to the arteries, the veins, and the abdominal organs. Although 
Hippocrates, who observed that liquid within an air-distended 
pleural cavity splashed audibly when the subject's body was suddenly 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 23 

shaken, was, in a strict sense, the first to practise auscultation, this 
procedure did not enjoy clinical vogue until the time of Laen- 
nec's publication, in 1819, of his Traite de V Auscultation mediate. In 
this masterpiece Laennec described his new invention, the stetho- 
scope, and dealt with the mechanism of auscultatory signs and their 
application, especially to diseases of the heart and the lungs, his 
conclusions upon these subjects becoming the acknowledged standard 
upon which subsequent studies were based. Of the many investi- 
gators to whom our present knowledge of auscultation is due, the 
names of Skoda, of Gerhardt, of Traube, and of Wintrich deserve 
noteworthy prominence. 

Auscultation, like percussion, may be either mediate or immediate, 
according to whether or not a stethoscope is employed, and of these 
two methods, the former is chosen in the great majority of routine 
examinations. In the exceptional instance, however, the naked ear 
appreciates certain sounds that are ill defined, if not quite imper- 
ceptible, with a stethoscope, so that to be equal to emergencies of 
this sort one must train one's self in the technic of both methods of 
auscultation. As Connor has pointed out, faint, high-pitched sounds 
are indifferently transmitted by closed tubes, particularly by tubes 
with flexible walls, from which fact it follows that certain cardiac 
murmurs of high pitch, blowing quality, and feeble intensity, as well 
as vesicular sounds of similar characteristics, are heard more 
clearly by auscultation with the naked ear than by using a stetho- 
scope, particularly one of the binaural pattern with two flexible 
rubber ear-tubes. 

Stethoscopic auscultation is of value chiefly in the investigation 
of circumscribed lesions of the respiratory, cardiovascular, and 
abdominal organs, since under such circumstances it is important 
to exclude every extraneous noise interfering with the peculiarities 
of the sound under analysis. Owing to their contour, certain 
areas of the body (i. e., the supraclavicular and infraclavicular fossae 
and the upper axillae) can be examined satisfactorily only with a 
stethoscope, while this instrument also comes into play when the 
patient's modesty, or perchance disregard of personal hygiene, forbids 
the direct application of the ear to the body, even if some covering be 
interposed. 

The Choice of a Stethoscope. — In the practice of mediate auscul- 
tation the choice of that form of stethoscope best suited to the needs 
of the user is the first essential of success. Naturally, this question 
must be decided largely upon personal grounds, although in the 
selection due weight should be given to certain acknowledged advan- 
tages peculiar to the various patterns of the instrument. 



24 



PHYSICAL DIAGNOSIS 



Two forms of stethoscopes are in general use — the binaural or 
double, modified to a greater or less extent from the design originally 
suggested by Camman; and the monaural or single, modeled after 
the original instrument invented by Laennec. The binaural instru- 
ments designed by Bowles, by Sansom, and by Arnold are well 
adapted to general clinical work, while Hawksley's monaural stetho- 
scope is the simplest and most 
convenient pattern of this type of 
instrument. 

The Bowles stethoscope consists 
of a steel, cupped chest-piece, fitted 
with a hard-rubber diaphragm, and 
communicating, by means of flexi- 
ble rubber tubing and a Y-coupling, 
with two metal conducting tubes 
provided with ear-pieces and con- 
nected by an adjustable steel spring 
(Fig. 5) . The standard disc-shaped 
chest-piece is made in two sizes, of 
which the smaller is preferable, 
owing to its restriction of the aus- 
cultatory area and to its accurate 
adaptation to depressed areas, such 
as the intercostal and supraclavic- 
ular spaces. For such purposes the 
small disc is just as satisfactory as 
the special "flat-iron" chest-piece 
devised for this sort of work. 
Bowles's stethoscope is convertible 
into an ordinary binaural by re- 
placing the metal chest-piece by a 
hard-rubber bell, also furnished 
with the instrument. 

Personally, the author prefers to 
use a Bowles stethoscope, equipped 
with soft-rubber ear-pieces, 1 a ij- 
mcn (3-75 cm.) rubber-capped disc, and 15-inch (37.5 cm.) lengths 
of the best grade of flexible catheter tubing (No. 14, E). The 
rubber cap, which prevents slipping of the chest-piece and nega- 
tives metallic tones, can be cemented to the disc with strong fish- 
glue. The catheter tubing, of the dimensions specified, is a perfect 
1 Made by C. H. Liverpool & Co., Boston, Mass. 




Fig. 5. — The Bowles stethoscope. 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 25 

conductor of sounds, and so flexible that it cannot kink. It is suffi- 
ciently long to allow adjustment of the chest-piece to any part of 
the back of a patient lying in dorsal decubitus, without disturbing 
the subject — a distinct advantage when examining a bed-ridden 
person too ill to be turned on the side. Thus equipped (Fig. 5), the 




Fig. 6. — Sansom's binaural stethoscope. Fig. 7. — Arnold's phonophore, 

instrument can be depended upon to amplify sounds without undue 
exaggeration, to conduct them with great purity and clearness, and 
to facilitate the analysis of circumscribed adventitious sounds. 

Sansorn's stethoscope (Fig. 6) embodies all the good points of the 
older types of binaural stethoscope, none of which, it may be added, 
is so satisfactory for routine work as the instrument devised by Mr. 



26 PHYSICAL DIAGNOSIS 

Bowles. All follow the same general principle — having a metal 
frame adjusted to the examiner's head by the pressure of a spring, 
and provided with ear-pieces and conducting tubes terminating in 
a chest-piece made of hard rubber, of wood, or of metal. In most 
binaurals the metal work and the rubber tubing are too light, the 
ear-pieces ill fitting, the chest-pieces defective, and the springs 
difficult to adjust properly. If a folding stethoscope (Fig. 6) be 
preferred, one should take care to select a model that can be opened 
and closed without straining the spring and frame, and that is pro- 
vided with a spring joint of stout construction and of firm locking 
action which does not rattle when the instrument is in use. 

Arnold's phonophore (Fig. 7), made in both binaural and mon- 
aural models, is especially helpful in listening to faint high-pitched 
sounds, which, as a rule, it transmits very clearly ; to other sounds, how- 
ever, this instrument seems to lend a hollow, somewhat metallic 
quality, and, to one unaccustomed to its use, an unnatural intensity. 
The phonophore is excellently made, having soft-rubber ear-pieces, 
heavy metal and rubber tubing, and a resonating steel chest-piece 
the sharp edge of which is fitted with a rubber cushion. 

The differential stethoscope is a form of instrument equipped with 
two separate chest-pieces communicating, by individual conducting 
tubes, one with the right and the other with the left ear of the auscul- 
tator. It is of service, say those who use it, in timing and in detecting 
quality differences of cardiac murmurs produced synchronously at 
different valve areas, by applying one chest-piece to one area and 
the other to another locality, and discrimi- 
nating between the differences in the tone 
and rhythm of each. 

iHawksley's monaural stethoscope (Fig. 8) 
consists of a hard-rubber ear-plate screwed 
into a rigid metal tube flaring at its other 
extremity into a bell-shaped chest-piece, or 
fitted with a detachable bell made of vul- 
canite or of ebony. This pattern of stetho- 
scope is preferred by some clinicians, 

notably by those of the older school, who 
Fig. 8.— Hawksley's mon- , . V, *_ ... . , . . ' 

aural stethoscope. claim that it transmits sounds with more 

distinctness, greater purity, and less arti- 
ficial intensity than instruments of the binaural model. The 
single stethoscope, though excellent in some respects, is inconvenient 
and fatiguing to use while examining a patient confined to bed, 
and is unsuited for auscultating the upper thorax and the lower 



^ 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 27 

abdomen. It is not clear that the single stethoscope serves any 
purpose not better served by an instrument provided with flexible 
tubing and two ear-pieces. 

Technic. — The posture of the patient, dictated by the nature of 
the examination, should be as unconstrained, relaxed, and easy as 
possible. This is no minor essential, especially in a self-conscious, 
nervous, or feeble person, to whom even the simple procedure of 
auscultation may be an ordeal sufficient to excite unnatural breathing, 
artificial muscular rigidity, and curious cardiac irregularity, all of 
which defects are exaggerated by a constrained, uncomfortable posi- 
tion. As in percussing, auscultating should not be needlessly pro- 
longed. 

In mediate auscultation the stethoscope should be applied to the 
naked surface of the body, for, unless preternaturally gifted, the 
average physician is unable to detect delicate acoustic differences 
through the patient's clothing, the rustling and creaking and dulling 
effect of which may effectually modify, if not entirely mask, important 
auscultatory findings. 

The chest-piece of a binaural instrument should be applied 
lightly and evenly to the surface over the area under examina- 
tion, being approximated thereto by the pressure of one or two 
fingers, which must not bear too heavily, lest the undue pressure 
thus exerted extinguish certain ill-defined sounds audible only when 
the stethoscope rests lightly upon the surface. As Sewall points 
out, stethoscopic pressure with the chest-piece of an instrument 
designed to transmit purely by air conduction has a distinct effect 
upon the character of the auscultated sounds, which are made 
up of two separate components — visceral tones and mural vibra- 
tions. Of the two, the latter generally predominate, and are more 
or less effectually effaced by firm pressure. In general, stethoscopic 
pressure, when it does not quite annul the voice sounds and the 
respiratory murmur, dulls them, raises their pitch, and lends to 
them a tinge of the bronchial tone, modifications due perhaps to 
pressure-dampening of the fundamental lower vibrations of the 
parietes. This modification is particularly true when pressure is 
made over the low r er part of the thoracic w r all. Emerson has shown 
that sounds produced at the parietes (i. e., faint tones of the heart; 
indistinct murmurs of mitral obstruction; the fetal heart-beats) 
are easily damped by the pressure of the stethoscope, while cer- 
tain transmitted sounds (i. e., high-pitched rales; blowing cardiac 
murmurs) are made clearer thereby. With a monaural stethoscope, 
held in position by the pressure of the examiner's head, it is espe- 



28 PHYSICAL DIAGNOSIS 

daily difficult to observe these niceties of adjustment, and, moreover, 
when firm pressure is. necessary, the chest-piece is likely to indent 
the subject's chest and cause considerable discomfort. Whichever 
model is used, the chest-piece must be held snugly in contact with 
the skin, so that the auscultator will not be confused by hearing 
extrinsic noises, amazingly magnified, which otherwise leak in; in 
emaciated subjects and in those with very narrow interspaces it is 
sometimes necessary to use a soft-rubber chest-piece to insure an 
air-tight contact. 

Only the tyro need be warned against confusing with adventitious 
sounds certain rude, jarring noises due to slips in technic, such as 
movements of the examiner's fingers over the metal parts of the 
stethoscope, accidental contact of the rubber tubing with nearby 
objects, and friction between the chest-piece and a dry, hairy skin. 
In addition to these extrinsic sounds, one must recognize various 
noises produced by contraction and respiratory movements of the 
surface muscles, particularly of the upper anterior thorax. 

Transmanual auscultation, suggested by Riesman to facilitate the 
timing of cardiac murmurs, consists of auscultating through the 
hand laid over the precordia, whereby, if the apex-beat be palpable, 
it is possible to feel the systolic impact of the heart and to hear an 
endocardial murmur at the same time and place. With a Bowles 
stethoscope there is no difficulty in distinguishing cardiac sounds 
through the intervening hand, and this combined method of pal- 
pation and auscultation is of distinct value, especially in differen- 
tiating presystolic and systolic bruits generated at the mitral orifice 
of the heart. 

Acromion auscultation (Abrahams), with the bell of the stetho- 
scope applied to the outer end of the clavicle, is useful in studying 
obscure apical sounds which are amplified and well transmitted 
by the conducting properties of the underlying bone. 

The technic of immediate auscultation is obviously too simple to 
call for detailed description, though it is not, perhaps, out of place 
to suggest that the auscultator should invariably cover the region 
under examination with a thin towel or other suitable material 
before applying the ear to the part. 

Phonometry. — The method of phonometry, by means of which 
the examiner aims to ascertain the condition of different organs by 
the tone of a tuning-fork placed on the surface, deserves recognition 
as a useful clinical aid. As elaborated by Habershon, by Benedict, 
and more recently by Cantlie, the examiner auscultates with a bin- 
aural stethoscope over a solid or a hollow organ to the vibrations 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 20, 

of a tuning-fork applied to the surface of the body over such an 
organ, and systematically moved so as to cross its outer bounda- 
ries. When this occurs, the sound originally heard suddenly grows 
faint or is quite inaudible, as the vibrations pass from the auscul- 
tated area to neighboring parts, and the observer is thus enabled 
to delimit the part by pencilling upon the skin the points at which 
this change of sound occurs. A fork with a narrow blunt handle 
and with long vibrating prongs tuned to a note of G sharp serves 
best for general purposes. Tuning-fork auscultation is applied 
to the outlining of pleural effusions of fluid, and to delimiting solid 
organs such as the liver, the heart and the spleen, and air-filled 
viscera like the stomach and the large intestine. 

The term autophonometry is applicable to a procedure based 
upon vibrating sensations appreciated by the subject when the 
handle of a vibrating tuning-fork is applied to the surface of the 
body, this method having been used to demonstrate pulmonary 
consolidations, as well as in the study of certain lesions attended by 
diminished cutaneous sensibility. Stritch has shown that the patient 
feels these vibrations most distinctly when the instrument is placed 
over a dull area of the thorax, less distinctly when over an impaired 
area, and least over normal pulmonary resonance. When a tuning- 
fork is placed upon various subcutaneous bony prominences (i. e., 
the sternum, malleoli, styloid process of the ulna, and nails of the 
fingers and toes) the vibrating sense is commonly abolished, often 
before cutaneous sensibility is impaired, in patients affected with 
peripheral neuritis, locomotor ataxia, spinal caries, syphilis of the 
cord, and diabetes mellitus. 



THORACOMETRY AND CYRTOMETRY 

The tape-measure and calipers, which should be graduated in 
inches and in centimeters, are employed for measuring various cir- 
cumferences and diameters, especially of the thorax and abdomen, 
for ascertaining the size of surface lesions, and for defining the exact 
position of local physical signs with reference to fixed anatomic 
landmarks. 

Thoracometry, or mensuration of the thorax, has for its chief 
objects the determination of the girth and the several diameters of 
the chest. In taking the girth, the tape should incircle the chest 
horizontally at the level of the nipples, and the measurements noted 
during respiratory repose, extreme inspiration, and extreme ex- 
piration, the difference between the last two expressing the 



30 PHYSICAL DIAGNOSIS 

chest expansion, which ordinarily amounts to from two to five 
inches (5 to 12.5 cm.) in a healthy man. Various stethometers, 
indicating the thoracic excursions upon a graduated dial, are 
available for measuring the chest expansion, but the simple 
tape-line is quite as accurate as any of these instruments. Com- 
parative measurements of the two halves of the chest are made by 
half-circling each side from midsternum to midspine, care being 
taken to follow precisely the same horizontal level and to apply the 
tape with equal tension on both sides. In comparing the semi- 
circumferences thus obtained, allowance must be made, in right- 
handed persons, for at least a one-half inch (1.25 cm.) greater 
measurement on the right than on the left side. In measuring 
abdominal girths the tape is generally passed horizontally around 
the belly at the level of the umbilicus. 

It is convenient to take as the vertical diameter of the chest the dis- 
tance from the highest point of the axilla to the lowest level of the 
costal margin, and to measure the two horizontal diameters at the 
level of the nipples; the anteroposterior diameter is found by applying 
one point of the caliper to the median line of the sternum and the 
other point to a vertebral spine, and the transverse diameter by caliper- 
ing the chest between two corresponding points upon the lateral 
walls in the midaxillse. 

Cyrtometry, or the procedure of outlining body-curves, is applic- 
able chiefly to determining the shape of the thorax in cross-section. 
For this purpose numerous more or less elaborate cyrtometers have 
been devised, none of which is more satisfactory than a simple 
instrument made of two narrow, flat strips of soft lead, each two feet 
(60 cm.) in length, and hinged together with a bit of rubber tubing. 
Having adjusted this hinge to the spine, the chest is incircled hori- 
zontally by the strips, which, being flexible, can be molded accurately 
to the body; having thus taken an impression of the entire circum- 
ference of the chest, the strips are removed by slipping them from their 
rubber connection, each section retaining the contour of the surface 
to which it was molded. A pencil tracing of the strips after their 
removal gives a graphic transverse section of the chest, and may be 
the means of revealing deviations from the normal contour too trivial 
to attract attention on casual inspection. Cyrtometry is useful both 
as a means of initial diagnosis and in studying, from permanent 
records, the progress of thoracic development and retrogression in 
persons affected with chronic pulmonary lesions. 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 3 1 



SPHYGMOMANOMETRY 

Sphygmomanometry, or the instrumental estimation of the 
arterial blood-pressure, shows the degree of arterial tension with 
far greater accuracy than simple feeling of the pulse affords, and 
serves also to confirm the details of the sphygmographic tracings. 
The sphygmomanometer, used for gaging the tension, is based 
upon the principle of measuring with a manometer the degree of 
pressure required to obliterate the pulse of a part distal to a given 
point of constriction, the result being expressed- in millimeters of 
mercury. A pneumatic constricting armlet, an inflating apparatus, 
and a mercurial manometer comprise the essential working parts 
of the instrument, of which the model designed by Nicholson is 
well suited for clinical work, inasmuch as it registers both systolic 
and diastolic pressures, and is accurate, simple, and portable. 
Rogers' aneroid sphygmomanometer, which registers the pressure 
by an aneroid gage, is much simpler than any of the mercurial 
manometers, and is sufficiently accurate for routine clinical work. 
Hill and Barnard's sphygmometer is useful for determining 
roughly the systolic pressure, in much the same way that one some- 
times estimates a hemoglobin percentage with a Tallquist scale, 
instead of with a more elaborate hemoglobinometer. 1 

Technic of Sphygmomanometry.— The working parts of Nich- 
olson's sphygmomanometer are housed in a metal case, the lid of 
which, when raised, locks automatically and firmly supports the 
whole device (Fig. 9). When shut, the instrument fits into a 
leather case, with the armlet and inflating bulb, and can be con- 
veniently carried in a coat pocket. The apparatus consists of a 
steel mercury reservoir, fitted above with a metal Y-connection for 
the inflation device and terminating below in a glass mercury 
tube, alongside of which is mounted an adjustable scale showing 
millimeter divisions. A soft pneumatic armlet, for application to 
the patient's arm, is connected by rubber tubing to one end of the 
Y-connection, to the other end of which fits a tube leading from 
the inflation bulb, which carries a stop-cock and a delicate needle- 
valve for controlling the pressure within the armlet. Before ad- 
justing the latter it is customary in hospital work to place the 

1 Nicholson's sphygmomanometer (Precision Thermometer and Instrument 
Co., Philadelphia) costs $15.00; Rogers' (Taylor Instrument Companies, 
Rochester), $25.00; and Hill and Barnard's sphygmometer (J. J. Hicks, London) 
sells for $3.10 plus duty. The original Riva-Rocci sphygmomanometer, and 
the modifications thereof suggested by Erlanger, Mummery, Martin, and others 
can be furnished by Hawksley and Son, London. 



3 2 



PHYSICAL DIAGNOSIS 



subject in dorsal recumbency, with the arm, relaxed and bared to 
the shoulder, supported by a pillow at the level of the heart. The 
inflation device having been applied to the arm, with the rubber 
bag over the brachial artery, the remainder of the armlet is wound 
smoothly around the arm and the end tucked under the last turn, 
so as to hold it in place when pressure is established. The con- 




Fig. 9. — Nicholson's sphygmomanometer. The auscultatory method of estimating 

blood-pressure. 



nection between the inflation device and the mercury chamber 
having been made, the zero mark of the scale is adjusted to the 
level of the top of the mercury column in the glass tube, and 
inflation is begun, with the stop-cock parallel to the tube and 
the needle- valve closed. Air is thus forced into the armlet until 
the radial pulse, meanwhile being palpated with the examiner's dis- 
engaged hand, is extinguished. When the pulse at the wrist is no 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 33 

longer appreciable, the release valve is cautiously opened until 
the mercury column (now high in the tube) begins to fall. The level 
reached by the mercury column at the moment the pulse reappears 
indicates the systolic pressure, which in the healthy adult usually 
ranges between 120 and 140 mm., rarely exceeding the latter figure 
in a young man, and being from 25 to 50 points lower in children 
under two years old. In the adult the systolic pressure may be ap- 
proximated with fair accuracy by adding 100 to the subject's age. 

As the mercury falls its oscillations progressively increase to 
an acme and then diminish, the base line of the maximum oscil- 
lation being taken as the degree of diastolic pressure, which va- 
ries normally from about 90 to no mm. in adults, or approxi- 
mately 30 points lower than the systolic pressure. This read- 
ing should not be made until the mercury column has had time 
to adjust itself after each fall, several fluctuations being observed 
at the various levels. The difference between the systolic and the 
diastolic figures represents the pulse pressure, a value normally ap- 
proximating from 20 to 30 mm. 

The auscultatory method (Korotkow) has of recent years largely 
replaced the original palpatory or oscillatory technic, just de- 
scribed. It is carried out by stethoscopic auscultation of the 
artery at a point below the cuff, while gradually releasing the press- 
ure upon the vessel, the primary object being the detection of the 
following series of sounds as the compressed artery refills with 
blood, with the escape of air from the armlet: (1) A loud clear tone, 
coincident with the first inflow of blood into the relaxed vessel; 
(2) multiple murmurs generated by local blood eddies; (3) a second- 
ary sharp sound, changing gradually to (4) an indistinct dull tone, 
caused by mural vibrations and followed by (5) complete silence, 
as the normal relations of blood volume to vessel lumen are re- 
stored. The height of mercury column when the first clear tone 
is heard is taken as the systolic pressure, which by this method is 
some 10 or 15 points higher than by the palpatory; and the figure 
registered at the time of the dull, muffled tone is generally conceded 
to indicate the diastolic pressure. The special stethoscope and 
tambour 1 devised by Oliver is most useful in determining blood- 
pressures by the auscultatory method. 

Of the two methods of clinical sphygmomanometry, the palpatory 

is, on the whole, more convenient, definitely graphic, and less subject 

to errors due to extraneous sounds and to the examiner's personal 

equation. In some instances, moreover, it is quite impossible to 

1 Price, $6.25, duty paid (Hawksley & Son, London). 

3 



34 PHYSICAL DIAGNOSIS 

make auscultatory readings, and to the untrained ear the accurate 
detection of the fourth (diastolic) phase of muffled tone is difficult. 

Both the palpatory and the auscultatory methods fail when deal- 
ing with variable pressures, individual or grouped, such as respira- 
tory undulations and those referable to cardiac arh\1;hmias, not- 
ably in the habitually irregular pulse of auricular fibrillation. In 
such cases it is customary to average the figures of several readings, 
but this obviously allows but an approximate result. Kilgore's 
fractional method, designed to interpret accurately the average 
pressures of both effective and abortive pulse beats, is somewhat 
too complicated for routine clinical use. 

Rogers sphygmomanometer (Fig. 10) consists of an aneroid man- 
ometer registering on a dial reading from o to 300 millimeters Hg., 
and of an armlet containing a rubber pressure-bag and connecting, 
by two rubber tubes, with the gage and with an inflating bulb. 
The tube leading from the latter is provided with a release valve, 
for relieving the armlet compression. The armlet, to be applied 
like a roller bandage, is held in place by tucking the small free 
end under the preceding fold, the pressure produced by the in- 
flating bulb being sufficient to keep it snugly adjusted to the 
subject's arm during the observation. The aneroid gage is then 
suspended from a hook on the outer face of the armlet, and the 
two rubber tubes are connected, one with the gage and the other 
with the inflation bulb. To obtain the systolic pressure, the armlet 




Fig. 10. — Rogers' sphygmomanometer. The palpatory method of estimating blood- 
pressure. 

is inflated by means of the bulb until the compression thus pro- 
duced obliterates the radial pulse, after which slight additional pres- 
sure is added. Now, by careful manipulation of the release valve, 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION $$ 

air is permitted to escape until the radial beats reappear, the 
figure registered on the dial at this exact moment representing the 
systolic pressure. To gage the diastolic pressure the air is released 
very slowly until the dial indicates a maximum range of oscilla- 
tions, whereupon the valve is quickly closed, and the minimum oscil- 
lation figure taken as the diastolic value. Rogers' sphygmomanom- 
eter reads within about 5 mm. of the figures of the mercurial 
instruments, over which it possesses the advantages of greater 
simplicity, ease of operation, and adjustability for differing barom- 
etric conditions. 

Hill and Barnard's sphygmometer consists of a glass gage gradua- 
ated in millimeters, and fitted, by a short length of rubber tubing, to 






Fig. 11. — The Hill-Barnard sphygmometer. 

a small rubber ball contained in a silk bag (Fig. 11). The gage is 
closed at one end by a metal cap pierced by a small orifice, which, 
by manipulating a screw, can be opened and closed. By means of this 
device a fluid meniscus can be produced within the lumen of the 
tube by placing its open end in water (or in ink) and screwing the 
column up and down until the top of the fluid reaches the zero mark. 
This accomplished, the rubber ball is distended with air, connected 
with the gage, and, covered with the palm of one hand, pressed down 



$6 PHYSICAL DIAGNOSIS 

firmly upon the subject's radial artery, the beats of this vessel being 
meanwhile felt with a finger of the examiner's other hand at a point 
peripheral to the rubber ball. The figure indicated by the fluid 
when the radial pulse is obliterated is taken as the systolic pressure. 
Hill and Barnard's instrument is not, of course, intended to do the 
work of the more accurate armlet-and-bulb sphygmomanometer, but 
its simplicity and extreme compactness recommend its employment 
when only a general idea of the blood-pressure value is desired, and 
under circumstances when a more elaborate method of sphygmo- 
manometry is impracticable. 

To insure accuracy, the blood-pressure should be investigated 
only when the subject is absolutely at rest, both physically and 
mentally, for no reading shows a true value unless obtained when 
the influence of transient circulatory stimuli can be excluded — mus- 
cular tension, intellectual effort, excitement, fear, all raise arterial 
pressure. Smoking a strong cigar may do the same, but alcohol 
has no material effect, save when taken too liberally, in which event 
the pressure falls perceptibly. Comparative estimates should be 
made under precisely similar conditions, relating especially to the 
subject's posture, to the time of day, and to the technic of the 
armlet application and other details. 

The practical application of sphygmomanometry and the patho- 
logic variations of arterial blood-pressure are considered subse- 
quently. It is sufficient here to associate hypertension with arterio- 
sclerosis, cardiac hypertrophy, renal sclerosis, and the toxic states 
attending gout, plumbism, syphilis, and other specific infections. 
Prominent factors of hypotension include shock, hemorrhage, vom- 
iting, diarrhea, anemia, enteric fever, tuberculosis, and various 
lesions of the heart marked by myocardial enfeeblement and 
dilatation. In the symptom-complex described by Ferry as "mal 
d'Aviateur" extreme hypotension with fatigue of the cardiovascu- 
lar system occurs in aviators, especially during the flier's ascent, 
as a result of the demands made upon the heart in adapting itself 
to varying atmospheric pressures. 

The term "energy index" (Barach) is used to indicate the total 
efforts per minute exerted by the cardiovascular system. This 
figure, which in health approximates 20,000 mm. of mercury, is 
calculated by multiplying the sum of the systolic and the diastolic 
pressures by the pulse-rate. Tigerstedt judges the actual pumping 
efficiency of the heart by dividing the pulse-pressure by the sys- 
tolic pressure; the figure normally reads from 25 to 35 per cent. 

Hoffmann, in 1906, suggested the use of the sphygmomanometer 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 37 

in the study of the pulsus altemans (q. v.), in which type of arhyth- 
mia a systolic manometer pressure may be reached which obliter- 
ates the alternately feeble impulses, and thus halves the pulse- 
rate at the wrist. In such instances the auscultatory method of 
tonometry affords at high pressures but one-half the number of 
the tones audible when the armlet is deflated. 

Pseudo-alternation due to the alternation of premature systoles 
with normal beats cannot be differentiated from the true pulsus 
alternans without graphic records. Apparent alternation arising 
from a rapid respiratory rate is easily detected by directing the 
patient to stop breathing for a few seconds (P. D. White). 

By Oliver's method the venous pressure can be estimated merely 
by noting at what height above the level of the cardiac apex the 
veins on the dorsum of the hand collapse, when the hand, with 
fingers extended, is held vertically and slowly raised. If the sub- 
ject has prominent veins, it is easy to distinguish their sudden 
collapse, which occurs normally at a height of J inch above the 
apical level. The height, in inches, at which this occurs above the 
apex is multiplied by 2, 1 to indicate — and with surprising accuracy 
— the venous pressure in millimeters of mercury. 

Although no direct proof of a venomotor nervous system is 
available, recent physiologic work suggests the hypothesis that a 
mechanism of this sort exists, comparable to the general vasomotor 
system (Yandell Henderson). The studies of Hooker show that 
the normal venous pressure and the alterations in arterial pressure 
are independent. With laboratory instruments Howell approxi- 
mates the normal venous pressure of the adult at about 7.5 cm. of 
water; while Hooker's figures read 10 to 20 cm. during the day and 
7 to 8 cm. during sleep at night. High readings are common in 
arteriosclerosis and in the failing compensation of various cardiac 
diseases; well-compensated lesions, whether muscular or valvular, 
produce no deviation from the normal figure. 

SPHYGMOGRAPHY AND CARDIOGRAPHY 

Graphic records of arterial and venous pulse-waves, of the cardiac 
apex-beat, and of other pulsations upon the surface of the body are 
obtainable by the use of special instruments devised for the purpose 
of registering surface undulations. For recording these different 
pulsations synchronously, some form of polygraph is necessary, 

x One inch, or 25.5 mm., represents about 2 mm. Hg. (1.985), reckoning the 
specific gravity of the blood and of mercury as 1.060 and 13.57, respectively. 



^8 PHYSICAL DIAGNOSIS 

such an instrument consisting essentially of a series of delicate levers, 
each tipped with a stilet and attached to a separate tambour, com- 
municating by rubber tubing with a cup-shaped capsule or receiver, 
which, when placed over a pulsating area, transmits the undulations 
thereof to its respective stilet. The latter rests upon the surface of 
a strip of smoked paper, driven by clockwork at uniform speed past 
the stilet point, whose oscillations are thus scratched upon the car- 
bonized film as a graphic tracing. A chronograph, or time-marker, 
is also useful in accurately indicating the time-incidence of the several 
tracings. The polygram made in this manner is suitably labeled 
by writing upon its smoked surface with a dry point, after which 
is flooded with tincture of benzoin or with negative varnish, hung 
up until dry, and subsequently filed with the case-history. 

Technic of Sphygmocardiography. — Of the several polygraphs 
now in vogue, Jaquet's model is to be preferred for clinical work if 
its high cost is not prohibitive, 1 since this instrument is compact, 
comparatively easy to operate, and capable of registering three 
synchronous tracings, which, though they may seem miniatures of 
those made by a large laboratory kymograph, show all essential 
details. Marey's polygraph, 2 practically unused in this country, 
is an accurate, though somewhat bulky, instrument, of more moderate 
price. Gibson's clinical polygraph, 3 which takes four simultaneous 
ink-tracings on glazed paper, is even more expensive than either of 
the two just mentioned. Dudgeon's sphygmograph, 4 adapted to 
recording but a single tracing, is used for making sphygmograms of 
the radial pulse. Equipped with Mackenzie's polygraph attach- 
ment, it will serve to register synchronously the radial beat and one 
other pulsating area, such as the jugular vein, the cardiac apex, or 
an aneurism. Mackenzie's ink polygraph 5 traces three separate 
records upon a strip of white paper. 

Jaquefs sphygmocardiograph (Fig. 12) is provided with a small 
metal plate which rests upon the subject's radial artery, and is 
attached to a delicate lever system carrying at its free end a light 
stilet for registering the movements of the radial pulse; a second 
stilet and lever system plays upon a tambour on the instrument, 
and leads, by a rubber tube, to a special receiver designed for the 

1 Price, $130.00, duty paid (Arthur H. Thomas Co., Philadelphia). 
2 Price, $120.00, duty paid (Charles Verdin, Paris). 

3 Price, $146.40, duty paid (T. Hawksley, London). 

4 Price, $20.00, duty paid (T. Hawksley; also J. J. Hicks, London). Biggs's 
time-marker, registering one-fifth second intervals, and designed for attach- 
ment to Dudgeon's sphygmograph, is furnished, at a cost of $9.00, by Messrs. 
G. Horstmann and Sons, Bath, England. 

6 Price, $84.00, duty paid (S. Shaw, Padiham, England). 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 39 



cardiac apex (or other surface pulsation), being adjusted thereto by 
a chest-strap; a third registering mechanism, of similar construc- 
tion, communicates with a cup-shaped receiver used for transmit- 
ting the jugular impulse. The three stilets simultaneously register 
upon a strip of smoked paper, which, by means of a roller and 
guide wheels revolved by clockwork, travels past the writing 
points so as to register their oscillations, definite time intervals 
meanwhile being marked by a chronograph stilet. The driving 
and time-marking mechanisms are controlled by levers, and the 
pressure of the radial plate is regulated by a milled screw. 




Fig. 12. — Jaquet's sphygmocardiograpti. 

Having fitted the cardiac receiver to the apex-beat and strapped 
the frame of the instrument snugly to the patient's wrist, as shown 
by the illustration (Fig. 12), the leather cuff is adjusted so as to 
bring the metal plate beneath the frame directly over the radial 
pulse-beat, the site of which has been previously marked with an 
anilin pencil. The smoked paper is then inserted between the roller 
and guide wheels, and the clockwork started in order to carry the 
strip along until the three stilets rest upon its surface, when its prog- 
ress is halted. The cardiac receiver is connected with its appropriate 
tambour, and the jugular receiver placed in position and similarly 
coupled to the instrument. When the three stilets rise and fall with 



40 PHYSICAL DIAGNOSIS 

proper amplitude, indicating satisfactory registry of the different 
undulations, the operator starts the chronograph and again sets the 
paper strip in motion and allows it to run its entire length, while an 
assistant catches the tracing as it passes from the roller and guide 
wheels, so that it emerges smoothly and evenly from the instrument. 
Having finished the tracing, the driving power is stopped and the 
strip benzoinated or varnished, as described above. 

Dudgeon's sphymograph, for tracing the radial pulse-waves, is pro- 
vided with a single lever mechanism similar to the corresponding 
arm of the sphygmocardiograph, for which, indeed, Dudgeon's device 
served as a model to be elaborated by the incorporation of additional 
stilets, receivers, and a chronograph. The accompanying picture 
(Fig. 13) shows the correct adjustment of the sphygmograph, held 




Fig. 13- — Dudgeon's sphygmograph. 

in position by a band and clamp, so that the metal plate of the register- 
ing lever presses upon the exact point where the radial artery beats 
most forcibly. Substitution of the standard metal plate by a slightly 
larger one attached to a more resilient spring has given, in the author's 
hands, much more satisfactory tracings than can be obtained with the 
original model of the instrument. It also simplifies the technic to 
tie the sphygmograph to the wrist with a flat elastic band, as Mac- 
kenzie advises, rather than to attempt to hold it in place by means 
of the orthodox strap and clamp. Glover uses an ordinary tourni- 
quet fitted with a cloth band, to each free end of which is sewed 
a metal clip, to be inserted into the slots where the wrist-bands 
are attached in the original model. Having adjusted the instru- 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 4 1 

ment so as to establish correct oscillations of the stilet, the smoked 
paper strip is set in motion and the tracing completed in the manner 
noted above. 1 While this is taking place the patient's forearm 
should rest upon a firm table, being supported by folded towels or 
similar pads so placed that the limb is kept relaxed and immobile, 
while the fingers, held in a position of moderate flexion, likewise must 
be kept perfectly still. 



a S 



a 



s 







/~V 1 


Jugul 
vein 


'h vr 






Fig. 14- — Simultaneous tracings of the normal arterial, venous, and cardiac pulsa- 
tions (Sphygmocardiogram by Dr. G. Bachmann). 



Interpretation of the Normal Sphygmocardiogram. — The 

above diagram (Fig. 14) illustrates the normal undulations recorded 
by a simultaneous tracing of the pulsations of the carotid artery, the 
cardiac apex, and the right external jugular vein, the synchronous 
points on these three waves being marked by the numbered 
ordinate lines. 

The arterial sphygmogram, typified by the carotid tracing, shows 
an almost perpendicular upstroke (3) , due to a sudden rise of blood- 
pressure, followed by an oblique downstroke (4-5), corresponding to 
the fall of pressure. A line drawn through the lowest points of 

1 Tracings in ink on white paper can be made by fitting the Dudgeon stilet 
with Macfie's glass writing point, made by Messrs. Down Bros., 21 St. Thomas's 
Street, London. 



42 PHYSICAL DIAGNOSIS 

the upstrokes, termed the base line, normally follows a virtually 
horizontal course. The upstroke (anacrotic limb) is coincident 
with ventricular systole, the pulse- wave arising therefrom being so 
sharp and abrupt that it produces a continuous and almost vertical 
line on the sphygmogram. The downstroke (catacrotic limb) is 
much more oblique, for it mirrors the comparatively slow fall of blood- 
pressure, and this line shows two distinct undulations: one known 
as the tidal (predicrotic) wave (4), due to secondary contraction 
and expansion of the artery immediately after its systolic distention; 
and a second, termed the recoil (dicrotic) wave (5), caused by the 
recoil of the blood-column, whose retreat aorta ward is suddenly 
checked by the closure of the aortic valve. Apart from these two 
normal oscillations of the downstroke, this line may also show minia- 
ture waves referable to the inherent elasticity of the arterial wall. 
The apex of the normal arterial tracing, or the angle between the 
upstroke and the downstroke, is acute, while of the two minor 
downstroke waves, the recoil is more conspicuous than the tidal. 

The cardiogram, shown by the above tracing, consists fundamen- 
tally of a perpendicular upstroke (2-3) and an oblique downstroke 
(5). The former marks the beginning of ventricular systole, and 
may be preceded by a minor wave, due to systole of the left auri- 
cle; ordinarily, the cardiogram fails to show this auricular undula- 
tion, the immediately preceding diastolic phase of which is difficult, 
if not impossible, to register in finer detail. The summit beyond 
the apex (3) is known as the systolic plateau, and is formed by a 
gently sloping line, usually rippled by one or more subsidiary waves, 
due to ventricular contractions. Chronologically, the systolic plateau 
corresponds to the impact of the heart against the parietes during 
ventricular systole, and from this summit the downstroke drops, with 
moderate obliquity, to the base line. The curve rising immediately 
after the downstroke (5) coincides with ventricular diastole, the first 
part of this line timing the active, and the latter part the passive, 
period of this phase, which, graphically, is the actual beginning of 
the upstroke. 

The venous sphygmogram, illustrated by the jugular tracing, is 
composed of three distinct waves corresponding to various move- 
ments of the right side of the heart, and constituting the so-called 
" physiologic venous pulse." The first of these waves (a), the 
auricular or a-wave, is presystolic in time, being coincident with the 
contraction of the auricles, and is due to the centrifugal impact of the 
venous column consequent to the slowing and sudden arrest of its 
onward flow. The second wave (s), commonly termed the systolic, 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 43 

is synchronous with the beginning of ventricular systole, or with the 
so-called "protosystolic period" of this chamber, when the tricuspid 
valve suddenly projects into the cavity of the right auricle and thus 
creates a reverse wave in the veins. 1 The third wave (v), known 
as the ventricular, is also systolic in time, but it occurs distinctly 
later than its protosystolic predecessor, for it accompanies the latter 
phase of ventricular contraction. The peculiar double curve of this 
undulation is produced by the sudden upward movement of the tri- 
cuspid valve and by the ascent of the auriculoventricular diaphragm 
to its resting position — events consequent to the relaxation of the 
papillary muscles at that period when the intraventricular tension 
exceeds the intra-auricular. The notch after the a-wave (2) marks 
relaxation of the auricle; that following the s-wave (Af) indicates 
auricular diastole; and that succeeding the v-wave (Vf) designates 
ventricular diastole and the passive period of the cardiac cycle. 

Clinical Value of Sphygmocardiography. — Accurate technic 
and intelligent interpretation of the tracing together make this 
method of unquestionable value, the all-important personal equation 
receiving, of course, due consideration in the individual instance. 
To regard sphygmocardiography as a pleasing bedside pastime is 
perhaps as great an error as to expect a ready-made diagnosis from 
every smoked slip. The arterial pulse tracing neither can nor should 
supplant the trained ringer in studying the size, volume, and mural 
condition of the vessel, but it does provide a permanent record of the 
pulse's rate, force, and rhythm, which thus can be crystallized on a 
single slip of blackened paper, together with numerous minor oscilla- 
tions too delicate to be felt. Simultaneous tracings (i. e., carotid, 
jugular, and precordial) indicate, as no other method of research can, 
disturbances of the auriculoventricular relations, asynchronism of 
ventricular contraction, and other cardiac arhythmias for the diagno- 
sis of which a comparable sphygmogram is indispensable. 

The characteristics of individual pulse tracings and their diagnostic 
significance in certain cardiovascular disorders are detailed in Sections 
V. and VI. 



1 Mackenzie and his school term this second ascent (s) the " carotid wave," 
and attribute it to the communicated impact of the carotid artery. While ad- 
mitting that this may be one of the factors of the s-wave, the arterial impact 
cannot be the sole cause. The s-wave unquestionably precedes the systolic 
line of the carotid pulse in the majority of accurate kymograms ; it has been 
repeatedly traced under circumstances absolutely precluding every possibility 
of a transmitted arterial throb (Bard, Cushny, Morrow); and, moreover, its 
disappearance has been noted after experimental inhibition of the ventricle 
(Porter). 



44 



PHYSICAL DIAGNOSIS 



ELECTROCARDIOGRAPHY 

With the electrocardiograph it is possible to study graphically 
the electric currents generated by the contracting heart, and thus 
to identify with great accuracy certain cardiac irregularities, 
notably those due to defects of conductivity, to premature systoles 
of the auricles and ventricles, to sinus disorders, and to paroxys- 
mal tachycardia. 

The electrocardiograph now in general use was perfected by 
Einthoven, on lines originated by Kolliker and Miiller, in 1856, 




Fig. 15. — Cambridge electrocardiographic outfit. 

and consists essentially of a delicate filament of silvered quartz 
stretching between the poles of an electromagnet activated by a 
storage-battery and wired to electrodes attached to the subject. 1 
The current traversing this filament at right angles to the lines 
of force of the electromagnet's magnetic field deflects it according 
to the direction of the current. The shadows of these oscillations 



1 The duty-free price of the Edelmann electrocardiographic outfit with the 
Einthoven string galvanometer, electrodes, illuminating system, photographic 
registering apparatus, and other accessories is $1031; the Cambridge instru- 
ment, complete, costs $1611, duty free. (A. H. Thomas Co., Philadelphia.) 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 45 

obtained by illumination with an arc light and magnified by a 
Zeiss objective and a system of condensing lenses are focussed 
upon a photographic film, driven at fixed speed, which, after 
proper development, constitutes the clinical electrocardiogram. 
The delicate movements of the filament attributable to "skin 
currents" are compensated by projecting, by means of a rheostat, 
sufficient current from a dry cell exactly to neutralize such de- 
flections, and the tension and sensitiveness of the filament are also 
adjustable, usually so as to secure a 10-millimeter deflection with 
the passage of a 1 -millivolt current. 

The patient, who must be warm, relaxed, and absolutely at 
rest, is included in the electric circuit by electrodes commonly 
consisting of zinc vessels containing warm salt solution in which 
the extremities are immersed, or of strips of metal enveloped in 




Fig. 16. — Lewis's diagram of the string galvanometer: A, Microscope for observ- 
ing the movements of the string of silvered quartz (C) suspended in the field of the 
electromagnets (S N); a, direction of current's movements, at right angles to the mag- 
netic field; C F, electric light and condenser. 



absorbent material saturated with saline and applied to both 
arms and one leg of the subject. The course of the current thus 
led off is termed a "lead," or "derivation," designated by the 
Roman numerals I, II, III, etc., according to the parts of the 
patient to which the electrodes are attached. Kraus and Nicoli 
have plotted six different leads, all of which afford different elec- 



46 PHYSICAL DIAGNOSIS 

trocardiograms, but for clinical purposes only three are in general 
use, as follows: Lead I, current from right arm and left arm; 
lead II, current from right arm and left leg; and lead III, cur- 
rent from left arm and left leg. Lead II gives the most useful 
record in the majority of electrocardiograms (Fig. 16b). 

Interpretation of all of the electrocardiographic waves is still 
an unsettled point, but the correctness of Einthoven's conclusions 
as to the conspicuous deflections is generally conceded. These 
waves, with his letterings, represent auricular systole at P, ven- 
tricular systole at Q, R, S, T, the conduction of the auriculo- 
ventricular impulse from P to R, and the diastolic period between 
T and P (Fig. 16a). 

By means of these simple alphabetic symbols the following 
pathologic variations of sequence, size, and incidence of the 



« s 



Fig. 16a. — Diagram of the normal electrocardiogram: P, Auricular systole; P-R, 
conduction-time of impulse from auricle to ventricle (0.12 to 0.17 second); Q, beginning 
of ventricular systole; R, basal ventricular activity; S, apical ventricular activity; T, 
end of ventricular systole; T-R, diastolic period. 

principal waves of lead II of the electrocardiogram may be 
designated: 

i. Irregular incidence, but normal sequence, of waves: tachy- 
cardia; sinus arhythmia. 

2. Prolonged P-R interval: sluggish impulse conduction from 
sino-auricular node to ventricle. 

3. Prolonged Q-R-S complex: delayed impulse conduction 
through ventricle. 

4. Replacement of P-wave by fine oscillations : auricular fibril- 
lation. 

5. Multiple P-waves in R-T interval: auricular flutter. 

6. Small or inverted P-wave, with premature P-, R-, and T- 
waves: auricular premature systole. 

7. Large P-wave: auricular hypertrophy; left ventricular dila- 
tation. 

8. Large prolonged P-wave, with deep 5 depression: ventricu- 
lar premature systole. (P-wave inverted in lead III, if left- 
sided, and in lead I, if right-sided.) 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 47 

9. Small R- wave: ventricular hypertrophy. (i?-wave inverted 
in lead III, if left-sided, and in lead I, if right-sided.) 

10. Simple inversion of i?-wave: deep, forced inspiratory effort; 
subphrenic pressure. 





HI 



pM^lM 



^r 



Fig. 166. — Normal electrocardiogram. Leads I, II, and III of a normal heart. 

11. Small i?-wave: cardiac dilatation (inconstant). 

12. Large J- wave: vigorous ventricular contraction. 

13. Small or inverted T-wave: feeble ventricular contraction. 
The diagnostic value of the more specialized electrocardiograms 

in various lesions of the myocardium and of the cardiac valves 
is duly considered in Section VI (p. 405 et seq.). 

PARACENTESIS 

Pathologic fluids and other material for laboratory study are 
obtained by puncture, or paracentesis, made with a hollow needle or 
a small trocar, ordinarily attached to a small syringe or connected 
with a vacuum bottle, by means of which the specimen can be readily 
aspirated. It is a good rule always to be prepared, when the occasion 
arises, to remove a foreign fluid as soon as it is detected, so as to spare 
the patient a subsequent operation. In consequence, exploratory 
punctures, though primarily diagnostic, are likewise potentially 



48 



PHYSICAL DIAGNOSIS 



curative. In this manner pathologic fluids within the pleura, peri- 
cardium, and peritoneum, as well as the contents of cysts and 
abscesses, maybe evacuated; the spinal canal tapped; the spleen 
and liver explored; and occasionally the consistence and nature of 
obscure tumors determined. 

Technic. — Paracentesis must »be carried out under rigid asepsis, 
the field of operation being scrubbed with a i : iooo mercuric chlorid 
solution, cleaned with soap-suds, rubbed with alcohol, and douched 
with sterile water, after which it is swabbed with iodin, which is 
allowed to dry, with or without the application of a sterile dressing. 
The needle, syringe, and other apparatus are to be sterilized, prefer- 
ably by boiling, and the operator's hands must be surgically clean. 

The site of puncture having been chosen (v. i.), the needle is 
introduced steadily but rapidly, and without any boring or lateral 
twist, until a sensation of suddenly diminished resistance and free 




Fig- 17. — Aspiration syringe and needles. 

mobility is perceptible, indicating that the point has passed through 
the parietal structures. To prevent damage from too deep a punc- 
ture, the operator should grasp the needle with the thumb and fore- 
finger just above its point, while piercing the comparatively resistant 
tissues of the surface. After withdrawal of the needle the wound 
is dried, covered with a bit of sterile gauze or cotton, and sealed with 
aristol-collodion. Only exceptionally, as noted below, is general 
anesthesia indicated, local anesthesia by ethyl chlorid or by eucain 
being usually sufficient to deaden the pain of the puncture. 

For withdrawing a small amount of fluid it is best to use an explor- 
ing syringe of about 6 mils capacity, fitted by a length of flexible 
rubber tubing to a hollow needle, the length and caliber of which are 
regulated by the situation and nature of the lesion to be explored 
(Fig. 17). For routine work it is well to have needles of three 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 49 

different sizes: 56, 45, and 30 gage, and i\ inches (6.2 cm.), 3 
inches (7.5 cm.), and 3! inches (8.7 cm.) in length, respectively. In 
lieu of a special aspirator, an ordinary hypodermic needle may 
sometimes be employed with success. 

When considerable fluid is to be removed, it may be allowed to 
drain off spontaneously through a coarse hollow needle or cannula 
(30 to 36 gage), or aspirated into a vacuum bottle. For aspirating 
a large effusion most clinicians use Po tain's apparatus, consisting 
of a set of three hollow needles, a trocar-cannula, and a graduated 
vacuum bottle and exhaust pump (Fig. 18). To the bottle are 




Fig. 18. — Potain's aspirator. 



fitted two rubber tubes, each having a separate stop-cock, one tube 
leading to an aspirating needle and the other to the pump, used to 
create a partial vacuum within the bottle and thus to exert suction 
through the hollow needle. The latter, having been inserted to the 
proper jiepth, is connected with the aspirating bottle, from which 
most of the air has been pumped out, the vacuum thus created being 
maintained by the closure of both stop-cocks. Suction is established 
by opening the needle stop-cock (the pump-cock remaining closed) 
just sufficiently to start a slow flow of liquid into the bottle. If it be 
necessary to interrupt the aspiration for the purpose of decanting 



50 PHYSICAL DIAGNOSIS 

the fluid and reexhausting the air within the bottle, the needle-cock 
must remain closed meanwhile. Failure to insert the needle to a 
sufficient depth commonly accounts for a "dry tap," the remedy 
for which is obvious, while a sluggish, intermittent flow may be due 
to blocking of the needle's lumen by a flake of fibrin, to unusual 
thickness and viscidity of the exudate, or to feeble aspiration force. 
These last obstacles can generally be overcome by reinserting the 
needle in a different direction after having partly withdrawn it and 
cleared its bore with a sterile wire, by the use of a needle of larger 
caliber, or by exhausting more air from the bottle. Having finished 
the aspiration and measured the fluid withdrawn, a portion for subse- 
quent examination is poured into a sterile container, or the vacuum 
bottle itself is taken directly to the laboratory. 

The laboratory report should embody data relating to the following 
points: (a) The physical properties of the fluid — specific gravity, 
color, odor, transparency, consistence, coagulability, and amount 
of sediment; (b) chemic examination of the filtrate, including tests 
for albumin, serum-globulin, and mucin; for sugar and urea; and, 
occasionally, for sarcolactic acid, succinic acid, allantoin, and inosite; 
(c) microscopic examination, for the detection of blood-corpuscles, 
epithelial and endothelial cells, crystals, necrotic tissue, ray fungi, 
hydatid hooklets and membrane, trypanosomes, piroplasmas, ame- 
bas, and pathogenic bacteria, which, if not demonstrable by direct 
examination, may be identified by culture and by animal inocula- 
tion ; (d) cytodiagnosis, whereby the number and character of the cells 
in the fluid are determined. For the technical details of these 
procedures the reader should consult a treatise on clinical laboratory 
methods. 

Pleurocentesis. — Puncture of the pleural cavity usually calls 
for the. use of a rather coarse needle and a Potain aspirator, for in 
the majority of instances this operation is a curative measure, neces- 
sitating the removal of much fluid. The site of puncture is deter- 
mined by the size of the effusion, and should lie well below the upper 
level of the fluid. The sixth interspace in the anterior axillary line, 
the seventh interspace in the midaxillary line, and the eighth inter- 
space midway between the latter and the scapular line are the points 
of election suitable in most effusions of average extent (Fig. 19). 
Too high a puncture may lacerate the lung above the effusion, while 
if the needle be inserted at too low a. level, it may penetrate the com- 
plementary pleural space, or tear the diaphragm, the liver, or the 
spleen. 

If possible, the patient, who must limit respiratory excursions, 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 5 1 



should sit upright during the operation, with the arm of the affected 
side swung across the chest so that the hand rests upon the oppo- 
site shoulder, thus widening the intercostal spaces. The puncture 
site having been chosen, the needle should be thrust directly through 
the middle of the proper interspace, thus avoiding the possibility 
of wounding an intercostal artery and of lacerating the costal peri- 
ostium. The effusion must be aspirated slowly, for its sudden with- 
drawal is not unattended by risk, chiefly from the sudden recession 
of the dislocated heart and from abrupt refilling of the previously 

PP. 




^^r^f 



Fig. 1 8a. — Pleurocentesis. 



collapsed blood-vessels of the lung. Aside from sealing the punc- 
ture wound, the affected side requires no attention, for it seems 
better to permit free movement of the thorax than to restrict it by 
strapping, as was formerly considered good practice. After the 
patient has passed three or four days in bed subsequent to the para- 
centesis, it is advisable to hasten expansion of the deflated lung by 
means of respiratory exercises. This is accomplished preferably 
by the use of a Wolff apparatus, whereby the patient, by blowing 
a measured volume of water alternately from one bottle into another, 
exerts a respiratory effort against a given degree of resistance. 

In that type of encysted effusion known as " blocked " pleurisy 
(pleuresie bloquie) ordinary aspiration fails to liberate the fluid, in 



5- 



PHYSICAL DIAGNOSIS 



which event two needles may be used, one for drainage and the 
other for forcing sterile air into the pleural pocket, thus driving out 
the contained liquid. 

The amount of fluid to be withdrawn at one sitting depends essen- 
tially upon the manner in which the subject bears the aspiration; 
in general, however, the volume should be too little rather than too 
great. If all goes well, it is safe slowly to drain off at least a liter — 
if this much exists — or, in the case of a massive effusion, as much 
as one and one-half liters, removing the remainder a day or two later. 



Pericardium 




Pericardium 



Pleura 



Peritoneum 



Peritoneum 



Fig. 19. — Points of election for paracentesis of the thorax and abdomen. 

If the patient coughs, gasps, and complains of pain in the chest, 
faintness, and suffocation, and if the blood-pressure falls notably, 
the aspiration must be temporarily suspended, or, if these symptoms 
persist, permanently abandoned, at least for the time being. It 
is not always necessary to aspirate a large volume of intrapleural 
fluid, for the withdrawal of a small amount (10 to 20 mils) may 
stimulate absorption sufficiently to dispose of the remainder by 
way of the lymphatic apparatus. 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 53 

Artificial pneumothorax is a remote accident, and one arising only 
in consequence of gross carelessness — air cannot enter the pleura if 
the needle and bottle be properly connected, and if the needle stop- 
cock be opened only when a satisfactory vacuum exists within the 
bottle. To assure this last essential the suction power and the valve 
action of the bottle should always be tested with sterile water before 
using the instrument of the patient. Sudden death of the subject 
during paracentesis, a most unusual accident, has been referred to 
extreme inhibition of the heart* due to irritation of the vagus and 
to vasomotor and respiratory paralyses from grave depression of 
the vasomotor and respiratory centers. 

Capps and Lewis have drawn attention to the danger of exciting 
a vasodilator reflex by irritation of the pleura, in consequence 
of which death may occur after a period of rapid and extreme 
decline of arterial tension, attended by shallow and hurried respira- 
tion and by other symptoms of collapse. Such an accident should 
be guarded against by making the puncture with great care and 
by avoiding unnecessarily deep penetration and irritation of the 
pleura with the needle; the emergency, should it arise, is best 
treated by adrenalin transfusion. 

A form of auto toxemia resembling so-called "serum illness," 
and characterized by albuminuria, fever, arthritis, and urticarial 
rashes, is a very remote sequel to pleural paracentesis. Albuminous 
expectoration also may follow the operation, but this accident need 
not be feared if the fluid has been drained off slowly and with care. 

Examination of a pleural fluid has for its chief object the differ- 
entiation of an edematous transudate from an inflammatory exu- 
date, both of which may have precisely the same transparency and 
yellowish hue, yet within certain limits are distinguishable by differ- 
ences in specific gravity, protein content, coagulability, and micro- 
scopic elements. A transudate, which resembles lymph, usually 
has a specific gravity of 1015 or lower, contains not more than 2.5 
per cent, of albumin, and, unless mixed with blood, does not coagu- 
late spontaneously. Microscopically, it shows little or no fibrin 
and a few endothelial cells derived from the pleural wall; blood- 
cells are found, if hemorrhage coexists, and fat-droplets, if the fluid 
be chylous. An exudate generally shows a specific gravity of 1018 
or higher, contains at least 4 per cent, of albumin, and clots promptly 
and completely. Microscopically, a dense fibrin network is found, 
and also degenerated endothelium, leukocytes, erythrocytes, and 
perhaps cholesterin crystals; pathogenic bacteria may or may not be 
demonstrable in the stained specimen, according to the nature of 



54 PHYSICAL DIAGNOSIS 

the underlying innammatory process. Although difficult to apply 
clinically, Zagoumenny's rule generally holds true, viz., that the 
alkalinity of exudates is less than that of the patient's blood, while 
the alkalinity of transudates is about the same as. that of the blood. 

Some exudates are frankly purulent or putrid, and, therefore, 
undeniably of inflammatory and infectious origin; some are hemor- 
rhagic, in which case either a tuberculous or a cancerous factor may 
be at work; some are eosinophilic, as in tuberculosis, rheumatic 
fever, and a wide variety of other diseases ; and some are milky or 
opalescent, for which peculiarities the presence of fat-droplets or 
of delicate albumin granules may account. In general terms it is 
true that the protein content of both dropsical and inflammatory 
fluids largely depends upon the site of the effusion, and is higher, 
as a rule, in pleural fluids than in those drawn from the perito- 
neum. 

Cytodiagnosis is useful principally in determining the nature of a 
bacteria-free fluid, and is based upon investigation of the number 
and character of the cellular elements observed in a stained film of 
the effusion. The relative proportions of lymphocytes and polynu- 
clear leukocytes, and also the erythrocytes and the cells derived from 
endothelial surfaces and from neoplasms, serve as the criteria for 
deductions, which relate chiefly to the differentiation of tuberculous 
and non-tuberculous effusions. 

A differential count showing lymphocytosis, or a predominance of 
mononuclear leukocytes, suggests either a mild or a subsiding inflam- 
mation, or some non-inflammatory process. Chronic tuberculous 
exudates are thus characterized, save during their incipiency and 
when active inflammatory complications supervene, under which 
circumstances the polynuclears are unduly numerous. 

A count affording polynucleosis, or a preponderance of polynu- 
clear leukocytes, generally denotes a well-defined and active 
inflammation of acute infectious origin, due, for example, to strep- 
tococci, staphylococci, pneumococci, or meningococci, and if such 
a process be of striking intensity, there will possibly be many 
necrotic cells and much detritus. 

Endotheliocytosis, by which is meant an undue relative or absolute 
increase in the number of endothelial cells, is the general rule in 
non-inflammatory transudates, and in such fluids both lymphocytes 
and polynuclears, particularly the latter, are in the minority. 

The detection of cancer cells, many with mitotic figures therein, 
in a fluid that also contains small bits of tissue of distinctively can- 
cerous structure, points to the malignant origin of the effusion. 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 55 

Caution must be observed, in the absence of corroborative cyto- 
logic findings, in attempting to differentiate true cancer cells from 
endothelial elements, an unnatural number of which, free and en 
plaque, Sahli speaks of finding in most effusions of cancerous 
character. 

Inoscopy may demonstrate tubercle bacilli in an effusion giving 
negative bacteriologic findings when examined by ordinary methods 
of film-staining. The technic of inoscopy, as elaborated by Jousset, 
consists of digesting the coagulum of the suspected liquid with pepsin 
and hydrochloric acid, centrifugalizing the liquefied mass, and 
preparing films from the sediment, to be stained by the Ziehl-Gabbet 
method and examined microscopically. 

Pericardicentesis. — Puncture of the pericardial sac is not to be 
undertaken lightly, inasmuch as a slight technical slip may irrepar- 
ably damage the heart; but, with due care, the operation is* 
practically without danger. Curative pericardicentesis is indis- 
pensable in dealing with a bulky effusion showing no tendency to 
undergo resorption, and in a condition of this sort the physical signs 
are so unmistakable that a merely diagnostic puncture is neither 
indicated nor justified. 

With the subject sitting upright or semiprone and restricting 
respiratory movements as much as possible, the needle is introduced 
through the middle of an interspace at a point within the area of 
cardiac percussion flatness. The instrument is then pushed inward 
along a horizontal plane while piercing the muscle, after which its 
point is cautiously directed inward until a sense of abolished resist- 
ance marks its entrance to the pericardial sac. Ordinarily, the fifth 
left intercostal space betw r een the midclavicular line and the ex- 
treme outer limit of effusion flatness is by far the most satisfactory 
site for puncture, though some prefer the fourth or the fifth left 
interspace, either close to or at least one inch (2.5 cm.) from the 
sternal border, so as to clear the internal mammary artery, which 
parallels the breast-bone at a distance of from \ to \ inch (0.6- 
1.25 cm.) from its margin (Fig. 19). In a very large effusion 
the freest drainage is sometimes secured by tapping the pericardium 
through the fourth right interspace close to the sternum (Dobert), 
or through the left costoxiphoid angle (Osier), thrusting the needle 
upward and backward and hugging the costal margin. 

In order to avoid causing sudden relief of the extracardial pressure, 
the fluid must be drained away slowly and in limited amounts, not 
more, for example, than 3 or 4 ounces (90-120 mils) at a single 
seance, which may have to be repeated subsequently if the effusion 



56 



PHYSICAL DIAGNOSIS 



be of considerable volume. The wound made by the needle re- 
quires no attention other than the treatment advised above. 

Examination of the pericardial fluid, by the methods just 
alluded to, decides the type of the effusion in question, whether it 
be the dropsical serum of hydropericardium, the bloody effusion 
of hemopericardium, the milky liquid of chylopericardium, or the 
inflammatory exudate of pericarditis. The physical properties and 
other characteristics of liquid effusions obtained from the pericardial 




Fig. 19a. — Paracentesis abdominis. Inserting the trocar and cannula. 

sac, being essentially like those of corresponding pleural liquids, do 
not require separate consideration (v. s.). 

Paracentesis Abdominis. — Diagnostic puncture of the abdominal 
cavity is sometimes indicated in the investigation of abdominal cyst, 
circumscribed abscess, and solid tumor, and under such circum- 
stances the needle virtually fills the dual office of instrumental pal- 
pation and aspiration. Hydronephrosis, subphrenic abscess, and 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 57 



cysts of the ovary and pancreas may come within reach of the explor- 
ing needle, but it is safer to cut down on a distended gall-bladder 
than to attempt its puncture, owing to the tendency of bile to 
escape into the peritoneum after the withdrawal of the needle. In 
making the puncture the operator guides the instrument so that 
it unquestionably penetrates the mass aimed at, and in this attempt 
great care is to be observed to prevent peritoneal contamination, 
either through a breach in the punctured part, or by leakage of 




Fig. igb. — Paracentesis abdominis. Fluid draining away, with trocar withdrawn and 

cannula in position. 

infected material from the eye of the needle. The latter is used 
in connection with an aspiration syringe, and should be of small 
caliber (about 50 gage), of high tensile strength, and of sufficient 
length to penetrate deeply. In the diagnosis of pneumoperito- 
neum Herrick's method of paracentesis with a blunt trocar and 
laterally perforated cannula is good practice. The cannula, being 
connected by rubber tubing with a wash-bottle containing water, 



58 PHYSICAL DIAGNOSIS 

transfers the free peritoneal gas to the liquid, the bubbling of 
which gives an ocular proof of gas. 

Therapeutic puncture of the peritoneal cavity for the relief of 
ascites is usually made alongside the median line of the abdomen, 
at a point midway between the pubic symphysis and the umbilicus; 
or at Munro's point, midway between the umbilicus and the left 
anterior superior iliac spine (Fig. 19). Inasmuch as the deep epi- 
gastric artery lies dangerously close to the latter point, Lian's site 
of election for puncture (the junction of the outer and middle 
thirds of an umbilico-iliac line) may seem a safer situation for 
introducing the trocar. The patient should be placed in a sitting 
posture, or, if bed-ridden, propped up in a semireclining atti- 
tude, so as to favor gravitation of the fluid to the lowest level 
of the peritoneal cavity. Having found that the subject's bladder 
is empty, and that the intestines are out of the way, a sterile 
muslin binder is fitted snugly around the abdomen, by which 
device uniform parietal pressure is applied while the fluid is es- 
caping. This binder, reaching from the lower epigastrium to the 
pubis, should be provided with a window in front and with in- 
terlacing tails behind, the former corresponding to the field of 
operation and the latter being used for traction. The punc- 
ture is made with a trocar and cannula, the former being withdrawn 
when the peritoneal sac is entered, and the fluid allowed to flow 
through the tube into a receptacle beside the patient. As the transu- 
date drains off, commensurate support is given to the abdominal 
wall by an assistant who stands behind the patient and, by taking 
up the slack of the interlacing tails, keeps the binder tightly applied 
to the abdomen as its size diminishes. This not only facilitates the 
flow, but to some extent wards off troublesome syncope, due to the 
sudden rush of blood from the periphery to the overdilated, toneless 
abdominal vessels. Syncope from too rapid withdrawal of the 
fluid can be averted by the use of a cannula of proper size (about 
35 gage), and by stopping the flow with the finger, from time to time, 
should the patient complain of vertigo or faintness. An apparently 
dry abdomen sometimes still yields a surprisingly large quantity of 
fluid when the point of the cannula is directed downward and 
swept about, while the subject bends far forward, compresses the 
abdomen laterally with both hands, and contracts the abdominal 
muscles. After the cannula is removed and the wound sealed, as 
above directed, a tight abdominal binder is applied, and the patient 
put to bed for about twenty-four hours. 

Buth's method of gradual evacuation is suitable if one fears 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 59 

the effects of the pain of puncturing with a large trocar or the 
danger of shock from too rapid a drainage of a massive effusion. 
This calls for the use of a "capillary trocar" and a cannula about 
f inch (8 cm.) long and a diameter approximating -^o" inch (1 J mm.), 
with lateral perforations near the end introduced into the peri- 
toneum and with a bulbous extremity for attaching a rubber tube. 
The instrument having been introduced in the usual manner, its 
point is directed downward through the belly wall, and after 
withdrawing the trocar and fitting a length of drainage-tubing 
to the end of the cannula, the fluid is allowed to drain into a 
receptacle alongside the patient. The fluid, which if fibrinous 
will not flow at all through such a small cannula, is usually evacu- 
ated at the rate of from 1 to 1 \ quarts (1 to 1 J liters) per hour, and 
with a minimum of discomfort to the patient. 

Drainage of the abdominal cavity, if skilfully done, is quite with- 
out danger, and may be repeated time and again in the same indi- 
vidual with perfect immunity from by-effects, as many an old alco- 
holic with a hard liver can testify. Even in preantiseptic days the 
harmlessness of repeated punctures of the belly was recognized, if 
one may judge by Algernon Ashton's description of a century-old 
English epitaph, which naively sets forth that the deceased "was 
tapped 97 times, and had 461 gallons of water taken from her, 
without ever lamenting her case or fearing the operation." 

Examination of the fluid obtained by abdominal puncture aims 
to distinguish ascitic transudates from peritoneal exudates, by the 
criteria already mentioned (v. s.), and to identify fluids aspirated 
from ovarian, echinococcus, hydronephrotic, and, rarely, pancreatic 
cysts. 

Ovarian cysts have a most variable composition, their contained 
fluid being commonly viscid and turbid or colloid, but excep- 
tionally resembling a thin, watery transudate. The specific gravity 
ranges from about 1005 to 1050, according to the richness of the 
albumin content, and the color may be amber, greenish, brightly 
sanguineous, or chocolate brown. The cystic fluid is of alkaline 
reaction, and contains, in addition to albumin, metalbumin, the 
presence of which is believed to be diagnostic. In a questionable 
fluid the absence of fibrin points to an ovarian cyst rather than 
to ascites. Urea and uric acid are sometimes found in considerable 
amount, and microscopic examination shows blood-cells and blood- 
pigment, degenerated epithelium, and often colloid masses. In 
an ovarian dermoid, hairs, squamous epithelium, fat, and choles- 
terin are the significant findings. 



60 PHYSICAL DIAGNOSIS 

Echinococcus cysts yield a clear alkaline fluid having a specific 
gravity usually not exceeding ioio, and containing a large amount 
of sodium chlorid, little or no albumin, a variable quantity of glu- 
cose, and, sometimes, inosite and succinic acid. The foregoing 
composition of the cyst fluid is greatly altered should it be 
contaminated by pus or by blood, in the event of which the 
diagnosis must be made entirely with the microscope. This 
shows distinctive echinococcus scolices, hooklets derived there- 
from, and fragments of cyst membrane, with such minor find- 
ings as eosinophile cells, cholesterin and hematoidin crystals, and 
fatty cells. 

Fluid from hydronephrotic cysts, if uncontaminated, may be 
either clear and watery, or amber tinted and cloudy, and generally 
ranges in specific gravity from about ioio to 1015. The detection 
of renal epithelium in the fluid is proof positive of. hydronephrosis, 
while the presence of a considerable amount of urea and uric acid is 
suggestive, but not conclusive, since both these substances are 
commonly found in the contents of ovarian and pancreatic cysts, 
and urea is demonstrable in both inflammatory and mechanical 
effusions. Apart from these details, there is nothing to be learned 
from the microscopic examination. 

From a pancreatic cyst of recent origin and rapid development 
one expects to obtain an alkaline fluid of low specific gravity and 
hemorrhagic character, containing a characteristic tryptic ferment, 
owing to the presence of which the fluid, despite its alkaline reaction, 
has the property of digesting egg-albumen. This most distinctive 
proof of a pancreatic fluid is supplemented in some instances by 
the demonstration of diastatic and fat-splitting ferments, whose 
significance is, however, in nowise pathognomonic. In an old cyst 
the tryptic ferment is rarely obtained, for it tends to disappear 
as the lesion ages. Albumin, uric acid and urates, cholesterin, 
and blood-pigment are other common constituents of cysts of the 
pancreas. 

Lumbar Puncture. — This procedure, popularized by Quincke, 
consists of tapping the subarachnoid space below the termination of 
the spinal cord, with the dual object, diagnostically, of obtaining a 
sample of cerebrospinal fluid for examination and of determining 
the degree of intraspinal pressure. Therapeutically, lumbar punc- 
ture is a means of relieving undue cerebrospinal tension, of draining 
the spinal canal and irrigating it locally, of administering meningitis 
serum and salvarsanized blood-serum, and of producing spinal 
anesthesia. The puncture may be made either with a stilet 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 6l 

needle devised for the purpose, or with an ordinary hollow needle 
of about 45 gage and three or four inches (7.5 to 10 cm.) in 
length. 

The patient is placed in lateral decubitus, back toward the opera- 
tor, with thighs flexed upon the abdomen and trunk bent well for- 
ward so as to widen the intervertebral spaces. Or the patient 
may sit facing the back of a chair, with the trunk arched passively 
forward and the arms and legs relaxed. General anesthesia 




Fig. 19c. — Lumbar puncture. Inserting the needle in the fourth lumbar interspace. 

is usually indicated in young children, but in adults it is unneces- 
sary. By preference the puncture is made between the spines of 
the fourth and fifth lumbar vertebrae, for here the spinal cord, 
terminating at the level of the second lumbar vertebra, cannot be 
lacerated. The fourth lumbar interspace is crossed by a horizontal 
line connecting the highest points of the two iliac crests. At this 
level and at a point directly in the midspinal line the needle is 
thrust through the skin and cautiously pushed upward and inward 
until it enters the spinal canal, at a depth varying from about f inch 
to 1 § inches (2 to 4 cm.) in children, to twice these distances in 
adults. As a rule, the fluid drips from the needle as soon as the 
point enters the subarachnoid space, and can be collected in a sterile 
tube as it flows out, drop by drop. If aspiration be necessary, the 
suction must be very slow and gentle, for fear of mechanically 
injuring the delicate spinal structures. Danger of damage by the 
needle's point is minimized by using a flexible rubber coupling be- 



62 



PHYSICAL DIAGNOSIS 



tween the mouth of the needle and the syringe. A "dry tap'' may 
sometimes be made productive by cautiously withdrawing the 
needle a short distance and reinserting it, by moving the patient's 
head and neck backward and forward and straightening the spine, 
or by passing a sterile wire through the bore of the needle to dis- 
lodge clots and fibrin flakes therein. 

The old belief that the velocity of the issuing stream is a rough 
index to the pressure within the spinal canal needs revision, in 
the light of Orlando H. Petty's recent studies of the spinal fluid 
of a series of 50 normal children. These investigations conclu- 
sively prove that the rapidity with which the drops emerge from 
the needle bears no relation whatever to the intradural pressure. 




Fig. igd. — Lumbar puncture. Collecting the cerebrospinal fluid after paracentesis. 

as indicated by manometer readings, and that a forceful spurt of 
fluid is not incompatible with a decidedly low pressure, while, on 
the other hand, a slow dribbling of diminutive droplets may occur 
with hypertension. Deviations of pressure are detected accurately 
by a small mercury manometer, attached to the aspirating needle, 
and held during the reading at the exact level of the puncture site 
(Fig. ickz). The normal pressure of the cerebrospinal fluid ranges 
within wide limits, determined chiefly by the age of the subject to 
which it apparently stands in inverse ratio. Thus, Petty's figures 
for 17 healthy children aged from nine months to five years averaged 
22 mm. Hg., the minimum being 10 and the maximum 28: at the 
adolescent age (six to fourteen years) in 15 children the foregoing 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 63 

figures read 18, 10, and 28; and in 15 older subjects (fifteen to sixty 
years) 6, 22, and 10 were the comparative figures. 

When the operation is finished and the needle withdrawn, the 
puncture wound is dressed with sterile gauze or sealed with cotton 
and collodion, and the patient kept in bed for the ensuing twenty- 
four hours or longer. 




Fig. 10^. — Landon's spinal manometer. 



Normal cerebrospinal fluid, of which from 5 to 10 mils ordinarily 
can be withdrawn by lumbar puncture, is an alkaline fluid of low 
specific gravity (1006 to 1008), and having the transparent, limpid 
appearance of distilled water, or, less commonly, being of a faint 
yellowish hue. It contains a small amount of protein, chiefly in 
the form of serum-globulin, and also chlorids, traces of urea and 
cholin, and a copper-reducing substance akin to, if not identical 
with, glucose. Microscopically, an occasional endothelial cell and 



6a physical diagnosis 

leukocyte, and often numerous erythrocytes, derived from the punc- 
ture, are found. 

The volume of the fluid is generally increased, in some cases even 
a hundredfold, and its flow proportionately accelerated, in menin- 
gitis, hydrocephalus, intracranial tumor, paresis, and certain infectious 
diseases. It may be blood streaked as the result of apoplexy, turbid 
and yellow in purulent meningitis, yellowish-green in jaundice, and 
delicate blue after the administration of methylene-blue. The 
specific gravity of the fluid rises decidedly as the consequence of 
meningeal inflammation, and it is usually higher than normal in 
paretics. The chemic composition of the fluid deviates from the 
normal in certain disorders, and, in general terms, such variations 
are of diagnostic utility. The protein content, which tends to rise 
after repeated tappings, may also be excessive in lesions responsible 
for a large increase in the cellular elements of the fluid, but it cannot 
be held that the protein-cell relation is always constant or propor- 
tionate. Albumin is appreciably increased in purulent meningitis, 
paresis, intracranial tumor, and apoplexy. An undue amount of 
cholin in the cerebrospinal fluid indicates disintegration of nerve 
tissue, and in general paresis, epilepsy, multiple sclerosis, alcoholic 
neuritis, and beri-beri this product of decomposition is commonly 
encountered. The chlorids are diminished in uremia (Carrie-re), and 
in this intoxication there is usually an increase of the urea, albumin, 
phosphates, and sulphates of the fluid. The reducing agent nor- 
mally present in the cerebrospinal fluid is frequently absent in 
pyogenic meningitis and in cerebrospinal meningitis, but in the 
acute stages of tuberculous meningitis and in poliomyelitis it is 
demonstrable. In diabetes mellitus, as a rule, this substance is 
decidedly increased, usually in close relation to the degree of 
glycosuria. 

The potassium content of the cerebrospinal fluid obtained be- 
fore death is in general higher in acute than in chronic lesions of 
the cerebrospinal system, but no relation exists between the potas- 
sium content and the cellular richness and globulin reaction of this 
fluid (Rosenbloom; Andrews). 

The calcium content remains very constantly at 5.0 mg. per 
100 mils of fluid (approximately one-half that of normal blood 
plasma), and variations from this figure are seldom met with, even 
in extensive luetic lesions of the cerebrospinal system (Halverson 
and Bergeim). 

Cytodiagnosis is of some value in differentiating certain acute and 
chronic types of meningeal disease. Thus, when the clinical picture 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 65 

suggests acute meningitis, a lymphocytosis implies tuberculosis as 
the factor, rather than the meningococcus, pneumococcus, streptococ- 
cus, staphylococcus, or other bacteria, in all of which a polynucleosis 
is the rule. Meningi tides of long standing and those nearing recovery 
cannot, however, be judged by this criterion, for in such instances 
there is ordinarily a definite lymphocytosis. In cerebrospinal 
syphilis, tabes, paresis, uremia, and other lesions that excite infiltra- 
tion of the meninges a lymphocytosis is also to be expected. In view 
of the foregoing facts it is obvious that cytodiagnosis of the cerebro- 
spinal fluid can be relied on only when interpreted in relation with 
all the other clinical findings of the case in question. The detection 
of cancer-cells in the cerebrospinal fluid has led to the antemortem 
diagnosis of carcinoma of the central nervous system (Widal) . The 
presence of many erythrocytes and lymphocytes in a yellowish 
fluid of high coagulability is a syndrome suggestive both of dural 
sarcoma and of meningomyelitis. 

Baderiologic examination of the cerebrospinal fluid includes the 
microscopic study of stained cover-glass films prepared from the 
centrifugalized sediment, supplemented, in appropriate cases, by. 
suitable cultural methods. Thus one can differentiate with absolute 
surety true meningococcus cerebrospinal fever from meningi tides 
due to the streptococcus, staphylococcus, pneumococcus, tubercle 
bacillus, and other bacteria. The offending bacterium can usually 
be identified by direct examination of the stained specimen, animal 
inoculation being called for only exceptionally. Even in tuberculous 
meningitis, contrary to current belief, the tubercle bacillus is found 
in from 75 to 90 per cent, of all cases, if the spreads be made from 
the delicate coagulum of the fluid (G. Canby Robinson). In pneu- 
monia Rohdenburg reports a high percentage (87 per cent.) of 
positive cultures in fatal cases, with a fair proportion (34 per cent.) 
in those recovering. In trypanosomiasis the Trypanosome gam- 
biense persists in the spinal fluid long after it has been driven from 
the blood and the glands by the use of atoxyl. 

The presence of a positive Wassermann reaction in the cerebro- 
spinal fluid is of great value in the diagnosis of syphilis of the 
central nervous system, and in paresis and tabes a positive colloidal 
gold test is helpful. 

Visceral Paracentesis.— Exploratory puncture of the spleen has 
become a routine clinical measure among those who deal wdth trop- 
ical splenomegaly and with obscure malarial infections, and the pro- 
cedure is also of great utility in certain cases of abscess and of hyda- 
tid disease. In enteric fever splenic puncture is scarcely justifiable, 



66 PHYSICAL DIAGNOSIS 

in view of the adequacy of other less perilous methods of diagnosis. 
Hemophilia and active congestion of the organ forbid splenic punc- 
ture. Using a very delicate hollow needle (not larger than 56 gage), 
the spleen is pierced either through the tenth left intercostal space 
in the midaxillary line, or, if it be greatly enlarged, at a convenient 
point below the left costal margin. During the operation, which 
must be done quickly, the patient should hold his breath, so as to 
minimize the risk of tearing, with the point of the needle, the par- 
enchyma of the organ or its capsule. These possible accidents, 
which may be followed by hemorrhage, peritonitis, and even splenic 
rupture, are more prone to occur when the spleen is soft and friable, 
as in enteric fever, than when it is hard and compact, as in ague cake. 

Puncture of the liver is generally made under general anesthesia, 
the organ being entered by a very fine needle passed through a right 
lateral or posterior interspace, well below the upper level of hepatic 
flatness, i. e., the seventh or eighth interspace in the right axillary 
space. Hepatic puncture has settled the diagnosis in many a case 
of pyogenic or amebic abscess, and of echinococcus infection of the 
liver; it should not be attempted in acute yellow atrophy, nor under 
the circumstances noted above as contraindications to puncture of 
the spleen. 

Puncture of the kidney is attempted only when a large renal swell- 
ing can be made out just beneath the abdominal wall, exploratory 
laparotomy being a more satisfactory means of inquiry in most 
instances. 

Puncture of the lung is occasionally helpful in detecting and in 
orienting pulmonary and bronchiectatic cavities, and in obtaining 
therefrom secretion for laboratory examination. For this purpose 
a long, fine needle and aspiration syringe should be used, the puncture 
being made where the surface signs suggest an excavation, the subject 
meanwhile controlling thoracic movement. If the needle-point, 
after penetration of the lung, can be freely swept through a consider- 
able arc, a large cavity is suggested, though a surer guide is the aspir- 
ation of a large amount of offensive secretion; if, however, the patient 
has freely expectorated just before the paracentesis is made, a cavity 
may yield no fluid whatever. A bronchial or pulmonary cavity, 
rather than empyema, is indicated by the aspiration, from a compara- 
tively deep level, of a mixture of air and mucopus containing elastic 
fibers and other microscopic evidences of tissue disintegration. 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 67 

FLUOROSCOPY AND RADIOGRAPHY 

Examination by means of the Rontgen ray, though more often 
corroborative of other findings than primarily diagnostic, has a dis- 
tinct place in physical diagnosis which no student of this subject 
can afford to ignore. The average internist cannot hope, nor does 
he desire, to have more than a bowing acquaintance with x-ray tech- 
nic, but it is highly desirable that his familiarity with radioscopic 
shadows and radiographs should be sufficiently thorough to permit 
intelligent association of his clinical impressions with the views of 
the trained specialist in x-ray work. 

Technic. — Detailed consideration of x-ray technic and of the risks 
inseparable therefrom is not germane to the plan of this book, and 
for this information treatises dealing with this highly specialized 
subject should be consulted. It may, however, be stated that the 
equipment required for this work includes some source of electric 
current, derived from an ordinary incandescent-light service, from a 
storage battery, or from a static machine; a coil capable of converting 
this current into one of greatly increased power (save when the 
electric supply is generated by a static machine) ; and an x-ray tube, 
consisting of a glass vacuum bulb inclosing a positive and a negative 
pole, made of platinum and wired to the current generator. The 
current, passing through the tube, jumps the vacuum gap from the 
positive to the negative pole, and produces luminous rays having the 
property of penetrating ordinarily opaque substances and of creating 
shadows visible with the aid of a fluoroscope, and permanently record- 
able upon a sensitized photographic plate. 

Fluoroscopy. — The fluoroscope, devised for the direct inspection 
of the shadows during rontgenization, consists of a pyramidal hood 
with an apex provided with an opening for the observer's eyes and 
a base made of a fluorescent screen which becomes luminous when 
acted upon by x-rays. With the area to be examined interposed 
between the x-ray tube and the fluoroscope the shadows cast by dense 
substances within the body cavities and other parts are clearly visible 
upon the surface of the luminous screen. The examinations should, 
of course, be conducted in a dark-room, in which the examiner 
ought to remain long enough to acquire a keen perception of faint 
shadows, before attempting to judge them with the fluoroscope. 

Radiography. — Except when effusions are being investigated, in 
which event the upright position is preferable, radiographs of the 
chest and abdomen are made with the subject in recumbency, the 
body being turned so as to bring the lesion to be photographed 



68 PHYSICAL DIAGNOSIS 

directly over a sensitized plate placed beneath the adjacent parietal 
parts. In thoracic work the scapulae are to be swept outward by the 
patient clasping the hands over the head, and the subject cautioned 
to make as little respiratory movement as possible. The correct 
posture having been assumed, the x-ray tube is adjusted and the 
exposure made, the resulting negative and print therefrom being 
carefully examined, in the light of the other clinical findings, and 
with the aid of a skilled radiographer's opinion. ■ 

Applied to internal medicine, the Rontgen-ray is helpful chiefly 
in the examination of the thoracic organs, and in some instances 
lesions of the heart and great vessels, bronchopulmonary system, 
and mediastinum are revealed only by this means. In such exami- 
nations fluoroscopy is superior to radiography, for it is a compara- 
tively simple procedure to inspect the chest contents with a fluoro- 
scope, while a photographic negative takes longer to make, and, unless 
instantaneously exposed, is blurred by the cardiac and respiratory 
movements. In abdominal work, on the other hand, radiography 
usually gives more accurate data than the fluoroscope, but neither 
is dependable unless the gastro-intestinal tract is practically empty 
at the time of the examination. Recently great advances have been 
made in the differentiation of gastric and duodenal lesions by the 
study of serial radiographs made at fixed intervals after the pa- 
tient's ingestion of a draft of bismuth-buttermilk. The x-ray's 
field of usefulness in abdominal diagnosis also includes the detection 
of calculi, especially of the kidney and of the urinary bladder, and, 
with less certainty, of the gall-bladder and ducts. The shape and 
size of the abdominal organs, as well as the presence of new 
growths that may invade them and other intra-abdominal struc- 
tures, are also demonstrable by the x-ray. 

The normal and pathologic x-ray pictures of the thoracic and 
abdominal organs, and their application to the diagnosis of special 
lesions, are referred to later, in connection with other physical signs. 

THE TUBERCULIN REACTION 

Here may be mentioned the several types of the tuberculin reaction 
observed in different forms of tuberculosis, and, properly employed, 
capable of serving as valuable, sometimes indispensable, clues in 
the diagnosis of obscure cases. 

Koch's tuberculin test consists of the hypodermic injection of a 
definite quantity of tuberculin, whereby moderate fever and other 
systemic disturbances are produced in a tuberculous subject, whereas 



METHODS AND TECHNIC OF PHYSICAL EXAMINATION 69 

in a healthy person no appreciable symptoms arise. Ordinarily, 
this test is resorted to only after all other methods of diagnosis have 
failed, for there is always a possibility, remote though it be, that the 
injection of tuberculin, by profoundly depressing the body's resistance, 
may light up latent tuberculous foci. Koch's old tuberculin (T. O.) 
is generally used for diagnostic purposes, the conservative initial 
dose being 0.2 mg., which, if insufficient to cause a reaction, 
should be followed, at intervals of a few days, by successive doses 
of 1,3, and 5 mg., until a reaction occurs. Experience has shown 
that if this routine be followed by negative results, no reaction will 
occur with the higher dosage (10 mg.) advocated by some investi- 
gators. A positive reaction occurring after a second or a third 
injection has not the same clinical value as a primary positive 
finding, for the first injection may, by a sensitizing process, cause 
a non-tuberculous subject to react. 

The criterion of a positive tuberculin reaction is fever, which should 
amount to at least 1 J° F. within from ten to twenty-four hours after 
the injection; such by-effects as rigors, aching, nausea, vomiting, 
and hemoptysis, while suggestive, do not constitute, in the absence 
of a rise of temperature, a positive reaction. As a rule, the subject's 
fever and indisposition disappear within from twenty-four to thirty- 
six hours after their onset. 

The cutaneous tuberculin test -of von Pirquet relates to an 
afebrile local reaction produced in the tuberculous subject by inocu- 
lation of the skin with tuberculin, after the manner employed in cow- 
pox vaccination. The "vaccine" consists of Koch's old tuberculin, 
diluted with 1 part of a 5 per cent, solution of carbolic acid in glycerin 
and 2 parts of normal saline solution. Two drops of this mixture 
are placed on the skin of the arm, about 2 inches (5 cm.) apart, and 
through each drop an abrasion is made by means of a sterile needle. 
A control inoculation is then made in the neighborhood with normal 
saline solution. If the reaction be positive, the site of inoculation 
will show, within twenty-four or forty-eight hours, an areolated 
papule about one-half inch (1.25 cm.) in diameter, and of a bright 
red color, which later deepens, and, fading during the course of a 
few days, sometimes leaves a pigmented area at its site. Rarely, 
turbid vesicles appear, and occasionally a small urticarial patch 
springs up at the point of inoculation. The control inoculation, of 
course, shows none of the changes just noted. 

Von Pirquet's test is of little practical value in diagnosing tuber- 
culosis in the adult, since positive reactions are not unusual in 
those who have passed the age of puberty, despite the fact that the 



70 PHYSICAL DIAGNOSIS 

subject is symptomatically free from all tuberculous taint. This is 
as one would expect, since few of us reach this period of life without 
having been at some time infected with Koch's bacillus. In children 
the test is more useful, and its value increases in direct relation with 
the youth of the child. From these remarks it is obvious that the 
cutaneous reaction is a delicate indicator of latent tuberculosis, in 
which, it must be added, positive results are obtained much more 
constantly than in active lesions. 

Calmette's ophthalmoreaction is the specific conjunctivitis 
excited by the instillation of a weak solution of tuberculin in the eye 
of a tuberculous subject, no such reaction being produced by this 
test in a person free from tuberculous taint. One minim of a c.5 
per cent, glycerin-free solution of dry tuberculin 1 is dropped into 
the inner canthus of the eye, whereupon, if the subject be tuberculous, 
acute congestion of the conjunctiva, with redness and swelling of 
the lacrimal caruncle, develops, usually within from three to six 
hours after the instillation, and, finally, in intense reactions, the 
conjunctival surfaces become bathed with a profuse puriform exu- 
date within the next six hours or so. In the exceptional instance both 
eyes are inflamed (S. H. Long). The inflammation thus produced 
generally abates within twenty-four or thirty-six hours, and entirely 
disappears by the end of three or four days. It is attended by free 
lacrimation and by a sensation- of moderate heat and burning in the 
instilled eye. The ophthalmoreaction is contraindicated by any sort 
of ocular lesion whereby the integrity of the eye is impaired, nor is 
it to be employed when there is reason to suspect a very active form 
of tuberculosis, for here the unduly low conjunctival resistance plus 
the irritant effect of the tuberculin might lead to serious local damage. 
The aggravation of a preexisting ocular lesion by the instillation of 
tuberculin may result in violent conjunctivitis, iritis, corneal 
ulceration, or pannus. 

The intensity of the reaction has no fixed relation to the severity 
of the tuberculous infection: incipient and mild cases rarely fail to 
react, while only about 50 per cent, of severe infections are positive. 
A positive reaction obtained at a second test, in the eye unaffected 
by the primary instillation, is of no clinical value whatever, for under 
such circumstances the development of conjunctivitis indicates 
merely the local sensitizing action of the earlier instillation, whereby 

1 The test solution is marketed in glass capsules, and also in the form of 
discs, one of which, dissolved in 1 mil of sterile water, makes a 1 per cent, 
solution. For fear of exciting too violent a reaction it is better to use a tuber- 
culin solution of one-half this strength. 



METHODS AND TECHNTC OF PHYSICAL EXAMINATION 7 1 

the conjunctiva may react to tuberculin, even if the subject be per- 
fectly healthy. Conjunctival congestion, it is interesting to note, 
is lighted up by the subcutaneous injection of tuberculin in a patient 
having recently reacted to the ophthalmic test. 

Morons reaction consists of the eruption of pale or of red papules 
over a cutaneous area after the application thereto of an ointment 
made of 5 mils of old tuberculin and 5 gm. of anhydrous wool-fat. 
A reaction of this sort has virtually the same significance as a posi- 
tive von Pirquet's test. 



SECTION II 
EXAMINATION OF THE THORAX 




CLINICAL ANATOMY 

The thorax consists of a bony framework formed by the sternum, 
the ribs, the vertebrae, and their cartilages, invested by a musculature 
of varying density; it incloses the esophagus, trachea, bronchi, lungs, 
heart, and great vascular trunks, and surrounds at its base the import- 
ant viscera of the upper part of the abdominal cavity. The bony 
thorax is shaped like a truncated cone, whose superior aperture is 
formed by the upper border of the ster- 
num, the first ribs, and the first thoracic 
vertebra, the inferior aperture being floored 
by the diaphragm. A cross-section of 
the normal adult thorax is elliptical (Fig. 
20), the transverse axis being decidedly 
longer than the anteroposterior; in the 
young child, however, the two axes are 
F ota 2 nOTmISTtWx° n practically equal, and this is also the 
case in certain types of chest deformities 
resulting from pathologic processes. (See Pathologic Types of 
Thorax, p. 79.) 

The average vertical measurement of the normal chest is 13 inches 
(32.5 cm.) in men, and 11. 8 inches (29.5 cm.) in women, the antero- 
posterior diameters being 7.7 and 7 inches (19.2 and 17.5 cm.), 
and the transverse diameters 10.5 and 9.8 inches (26.2 and 24.5 cm.) 
for the respective sexes (Bessenen). Fourmentin's " thoracic index" 
(anteroposterior diameter x 100 -5- transverse diameter) equals, 
in the normal man, 72 (Woods Hutchinson). The normal chest 
expansion varies from 1^ to 4 or 5 inches (3.8 to 10 or 12.5 cm.), 
while the circumference, according to Otis's measurements, averages 
34 inches (85 cm.) in men and 29.5 inches (73.7 cm.) in women. 
The respiratory capacity of the average male thorax is approximately 
3.3 liters (201 cubic inches), or about 20 mils for each centimeter of 
stature. 
72 



EXAMINATION OF THE THORAX 73 

A perfectly symmetric chest is rare, although conspicuous devia- 
tions from the normal contour are seldom met with, except in those 
who have acquired local muscular overdevelopment, usually as the 
result of their occupation or a similar cause. The one-sided 
chest fulness of the blacksmith and of the iron puddler and the 
drooping shoulder of the hod-carrier are familiar types of this sort 
of asymmetry. Aside from such influences, however, the right half 
of the chest is generally somewhat larger than the left half in right- 
handed persons, and there are few adults, even in perfect health, 
that do not show a moderate dextral inclination of the dorsal spine. 
In those who are left-handed the asymmetry is, of course, left sided. 

NORMAL LANDMARKS 

Study of the thoracic organs is facilitated by the use of the normal 
landmarks, bony and muscular, upon the walls of the chest, as well 
as by the aid of a number of arbitrary lines drawn upon its surface. 
Having detected a given sign, it is first oriented in a certain area of 
the thorax, and then more accurately localized by determining its 
precise relation to one of these fixed anatomic landmarks and to a 
surface line. For example: "A systolic pulsation in the fifth left 
intercostal space, one-half inch to the right of the left midclavicular 
line," technically describes the situation of the normal apex-beat of 
the heart. 

The clavicles are conspicuous landmarks upon the anterior chest- 
wall: a moderate prominence of these bones is not incompatible 
with good health, and even bilateral deepening of the fossae above 
and below the collar-bones may exist, without the slightest implication 
of the pulmonary apices. Unilateral depression in one of these regions, 
on the contrary, is extremely significant of an apical lesion, especially 
if the sunken area expands laggingly and imperfectly during respira- 
tion. The sternal ends of the clavicles correspond to the level of the 
disc between the second and third thoracic vertebrae. The depressed 
area below the junction of the middle and outer thirds of the 
clavicle, between the pectoralis major and the deltoid muscles, is 
known as Mohrenheim's fossa (Fig. 21). 

Lloyd Jones has noted that in right-handed adults the right clavicle 
is tilted more than the left, that in the left-handed the left clavicle 
is tilted more than the right, and that in the ambidextrous the clavicles 
slope equally. 

The sternum, bounded above by the suprasternal notch and 
below by the "pit of the stomach" (scrobiculus cordis), is the seat 
of two important surface-markings: the angle of Louis (angulus 
Ludovici) and the xiphisternal joint (Fig. 21). The angle of Louis 



74 



PHYSICAL DIAGNOSIS 



is a transverse ridge, always palpable and usually visible, formed 
by the articular surfaces of the manubrium and the gladiolus, and 
corresponding in front to the level of the second costal cartilage, and 
behind to the third thoracic vertebra. Since this prominence indicates 
the position of the second rib, it serves as an accurate landmark in 
counting the ribs. The xiphisternal articulation (Fig. 21) is situated 
just below the sternal end of the seventh costal cartilages and cor- 
responds to the disc between the ninth and tenth thoracic vertebrae. 




'Suprasternal notch 



Supraclavicular fossa 


\^ 


«^f 






Infraclavicular 


^v 








(Mohrenheim's) fossa 












. 


Angle of Louis 


Sibson's furrow 






■ 




J 


angle 








Scrobiculus cordis 




1 








Base of costal arch 






,<M 





Fig. 21. — Normal thoracic landmarks 

The ribs and intercostal spaces are usually taken as the horizontal 
topographic lines, the number of an interspace being that of the rib 
immediately above it. Owing to the obliquity of the ribs, their 
sternal ends are at a lower level than their vertebral: the first rib in 
front is in the plane of the fourth rib behind, and the anterior level 
of each of the next five ribs (second to seventh, inclusive) corresponds 
to the posterior level of the fourth rib below it. The first seven (true) 
ribs articulate individually with the sternum, but the lower five (false) 
lack this direct attachment to the breast-bone. In the well-developed 
adult, the ribs are visible only upon the lateral walls of the lower 



EXAMINATION OF THE THORAX 75 

chest. The upper ribs run horizontally outward from their sternal 
attachments, but as the epigastrium is approached their obliquity 
increases, so that the epigastric or subcostal angle, formed by the 
substernal divergence of the costal margins, is approximately an 
angle of 70 ° (Fig. 21). With inspiration the subcostal angle is 
more obtuse than with expiration, owing to the exaggerated obliquity 
of the ribs during the latter period of breathing. 

In counting the ribs on the anterior chest-wall Louis' angle and the 
lower border of the pectoralis major muscle (Sibson's furrow) are 
accurate indices to the second and the fifth ribs, respectively. It is 
much easier, to find the first rib by counting upward from the former 
landmark than by direct palpation backward and downward under 
the clavicle. The lowest part of the costal arch corresponds to the 
cartilage of the tenth rib. Laterally, the highest visible slip of the 
serratus magnus muscle is a guide to the fifth rib. Posteriorly, the 
scapula extends from the second to the seventh rib inclusive, the 
inner end of its spine being at the level of the third thoracic spine 
and its inferior angle corresponding to the seventh thoracic ver- 
tebra. The scapulae do not stand out prominently from the normal 
thorax, but lie snugly against it. The "scaphoid scapula" 
(Graves), with concave vertebral borders, is generally considered 
a normal variation and not a developmental anomaly, as formerly 
believed. Other bony landmarks useful in counting the ribs 
in the back are the seventh cervical vertebral spine {vertebra 
prominens), directly below T which is the joint of the first thoracic 
vertebra and the first rib. The free tips of the eleventh and 
twelfth (floating) ribs correspond to the spines of the eleventh 
and twelfth thoracic vertebrae, and are palpable outside the 
erector spinae muscles. Each thoracic spine from the second to 
the ninth inclusive corresponds in number to that of the rib next 
below it serially ; the tenth spinous process is opposite the tenth 
interspace. 

The upper intercostal spaces, of which the second usually is the 
widest, are readily palpable, especially in front, but it is sometimes 
a difficult matter to feel the lower interspaces, owing to their narrow- 
ness. 

The nipple in a man usually lies between the fourth and the fifth 
ribs, about 4 inches (10 cm.) from the center of the sternum. A 
woman's nipple is situated somewhat below the center of the mam- 
mary gland, which covers the chest-wall from the second to the sixth 
or seventh ribs, and from the sternal border to the anterior limit 
of the axilla. The female nipple is not a reliable surface-marking, 
owing to the variable size and shape of a woman's breast. 



76 . PHYSICAL DIAGNOSIS 

TOPOGRAPHIC LINES AND AREAS 

In connection with the foregoing anatomic landmarks the clinician 
makes use of a number of imaginary vertical lines, drawn parallel 
to the long axis of the torso, these lines, in their order from sternum 
to spine,, being as follows: 

The midsternal (anterior median) line, passing through the 
middle of the sternum, from the cricoid cartilage above to the tip 
of the xiphoid appendix below. Prolonged downward, this line 
divides the abdomen laterally and ends in the middle of the symphysis 
pubis. 

The sternal (lateral sternal) line, paralleling the lateral border of 
the sternum, and continuous below with the line of the costal arch. 

The parasternal line, drawn midway between the sternal line and 

The midclavicular (mammillary, nipple) line, let fall from the 
middle of the clavicle. Projected downward this line crosses the 
costal arch at the level of the ninth costal cartilage, and is continuous 
with the vertical Poupart line, which terminates in the middle of 
Poupart's ligament. This line, although commonly termed " mam- 
millary," rarely passes through the nipple, frequently running wide 
of this point in the male, and almost invariably doing so in the female. 

The anterior axillary line, running downward from the anterior 
fold of the axilla. 

The midaxillary line, drawn from the middle or apex of the 
axilla. 

The posterior axillary line, dropped from the posterior fold cf the 
axilla. 

The scapular line, falling perpendicularly through the inferior 
angle of the scapula. 

The midspinal (posterior median) line, corresponding to the 
middle of the spinal column. 

For an ordinary clinical examination the ribs and interspaces are 
sufficiently definite horizontal landmarks, although in certain instances 
it may be advisable, for the sake of technical description, to localize 
a physical sign with relation to certain imaginary horizontal lines. 
Drawn across the long axis of the trunk, these lines may be indicated: 

The cricoclavicular line, drawn from the cricoid cartilage of the 
larynx to the point upon the clavicle crossed by the upward projection 
of the anterior axillary line. 

The clavicular line, following the course of the clavicles. 

The third costal line, drawn from the third chondrosternal 
articulation to the anterior axillary line. 





.- '" 










V 






\ 












\ 




^J 










s 




\ 


"? ■ ' 










i " 








^PPP- 


rr x ' x 


j 







y 



\ 





\ 


\ 


\ 


1 / / ' / \ \ v\ 




3> 


o 

o 

CO 


(73 


h >2?Si:Qo 




O 




n 
1 


:oclavic 

vicular 
Islernal 
nal 

asternal 
clavicu 
erior ax 

rd costa 


*J 








,— • gp t- 












OQ 








-i ,_l 







/ 






Sv. 


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i\ 


' 


?7- z 


:/: 


>• 



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?2> 



Axillary 



77 



78 



PHYSICAL DIAGNOSIS 



The sixth costal line, drawn from the sixth chondrosternal 
articulation to the posterior axillary line. 









tin 


f— — - ^s 


<p 


3a 


"5 


-J 




t^-^o>S-c^-^> 


EC; g 


2 













The line of the cos/a/ a/r^, continuous with the sternal line and 
following the costal margin. 

The infracostal line, connecting the lower borders of the tenth 
costal cartilages. 



EXAMINATION OF THE THORAX 79 

The scapular spinal line, corresponding to the spines of the 
scapulae. 

The infrascapular line, at the level of the inferior angles of the 
scapulae. 

The line of the twelfth thoracic vertebra, curving outward and 
downward from the spinous process of this bone to the posterior 
axillary line. 

The following topographic regions (Fig. 23) may be mapped out 
upon the surface of the chest by the use of the foregoing lines: 

The sternal region, corresponding to the sternum, extending verti- 
cally from the suprasternal notch to the tip of the xiphoid process, 
and horizontally between the sternal lines. 

The supraclavicular region, or the triangular space over and above 
the clavicles, bounded externally by the cricoclavicular lines. 

The infraclavicular region, bounded above by the clavicle, below 
by the third costal line, externally by the anterior axillary line, and 
internally by the sternal line. 

The mammary region, lying between the third and sixth costal, 
and the anterior axillary and sternal, lines. 

The hypochondriac or inframammary region, lying below the sixth 
costal line, being limited internally and below by the line of the 
costal margin, and externally by the anterior axillary line. 

The axillary region, extending from the apex of the axilla to the 
sixth costal line. 

The infra-axillary region, from the sixth costal line to the costal 
margin, the lateral boundaries of both axillary areas being the 
anterior and posterior axillary lines. 

The suprascapular and the scapular regions overlie the supra- 
spinous and the infraspinous fossae of the scapula respectively; the 
interscapular region includes that part of the back between the 
scapulae; and the infrascapular region extends, between the right 
and left posterior axillary lines, from the inferior scapular line to that 
of the twelfth thoracic vertebra. 

PATHOLOGIC TYPES OF THORAX 

Of the several types of bilateral abnormalities of the thorax, some 
are so constantly associated with definite diseases as to serve as 
almost certain clues to these conditions, while others betray simply 
retarded or erratic physical development. The first group includes 
the forms of chest peculiar to phthisis, to hypertrophic emphysema, 
to rickets, and to syringomyelia; the second group comprises those 



8o 



PHYSICAL DIAGNOSIS 



observed in the thin, undeveloped individual and in the woman that 
laces too tightly. 
The Phthisical Thorax (Pterygoid; Paralytic; Alar).— The 

typical chest of the phthisical subject appears long, emaciated, 
deficient in expansion, and often shows circumscribed areas of flatness 
and of retraction (Figs. 24 and 25). The common belief, current 
since the days of Galen, that the phthisical thorax is shallow and 
flat, is true of some cases, but in others, especially in those with lesions 
far advanced, the anteroposterior diameter is greater than normal 

and the transverse outline 
of the chest deep and 
round (Woods Hutchinson) 
(Fig. 26). 

The neck is likely to be 
long and slender, the larynx 
conspicuous, the clavicles 
prominent, and the supra- 
clavicular and infraclavic- 
ular areas abnormally and 
unequally deep. The angle 
of Louis forms a prominent 
transsternal ridge, and the 
ribs, separated by unusu- 
ally wide intercostal spaces, 
incline sharply downward 
from the sternum and as 
sharply bend upward again 
as they approach the spine. The subcostal angle, owing to this 
increased obliquity of the ribs, is extremely acute. The shoulders 
generally slope, and the scapulae, instead of hugging the back, stand 
out like a pair of wings — hence the term, "winged" or "alar" 
scapulae. The chest showing the foregoing group of changes has 
also been labeled the "expiratory form of thorax." 

The phthisical thorax must not be mistaken for the emaciated 
chest of a patient convalescent from some acute febrile disease, 
such as enteric fever; in the latter instance, while the emaciation of 
the thoracic parietes may be striking, the chest does not show the 
slightest evidence of actual structural deformity. 

The Emphysematous Thorax (Inflated, Barrel-chest). — The 
thorax of hypertrophic (large-lunged) emphysema is short, deep, 
overdistended, and frequently bulged out in the central portion, so 
that it conforms more or less to the shape of a cask — the so-called 




Fig. 24. — The thorax of incipient phthisis (Jef- 
ferson Hospital). 



EXAMINATION OF THE THORAX 



8l 



"barrel-chest" (Fig. 27). This peculiarity is most striking when 
the emphysematous enlargement affects especially the upper pul- 




Fig. 25. — The thorax of advanced phthisis (Philadelphia General Hospital). 



monary lobes, being less evident when the process is diffuse and when 
it implicates chiefly the lower part of the lungs. Fig. 20. shows a 
transverse section of the typical "barrel chest." 

The neck is usually short and thick, 
and the shoulders elevated, squarely set, 
and bent forward. The angle of Louis 
is prominent, the sternum distinctly pro- 
truded, and the upper intercostal spaces 
widened, while those ol the lower thorax 
are narrowed and drawn in during in- 
spiration. The ribs run horizontally 
from the sternum, and in consequence 
the subcostal angle is obtuse. The respiratory movements of the 
emphysematous chest are highly characteristic, the excursion being 




Fig. 26. — Transverse section of 
a phthisical thorax. 



82 



PHYSICAL DIAGNOSIS 



vertical and rigid, as if all the structures of the thorax were welded 
together and rose and fell en masse. 

The " inspiratory form of chest" is a term also applied to a thorax 
having these characteristics, and the presence of such a deformity 
is almost proof positive of hypertrophic pulmonary emphysema, 
although it must be borne in mind that these changes do not neces- 




Fig. 27. — Emphysematous thorax (Philadelphia General Hospital). 

sarily develop in every case. Kyphosis may superficially resemble 
the "barrel chest," but in ordinary "hump-back" the costosternal 
peculiarities and the vertical type of chest movements are absent. 

The Thorax of Atrophic Emphysema. — This is the small, con- 
tracted type of chest met with in subjects of atrophic (small-lunged) 
emphysema, and is the direct consequence of senile atrophy of the 
lungs. The thorax is abnormally diminutive, shallow, and peculiar!) 



EXAMINATION OF THE THORAX 



83 



deformed by bowing of the shoulders, by depression of the sternum, 
clavicles, and ribs, by exaggerated costal obliquity, and by narrow- 
ing of the lower interspaces. The respiratory excursion is greatly 



\ 







Fig. 28. — The thorax of atrophic emphysema (Jefferson Hospital). 



restricted, for the chest-wall is rigid, and inspiratory sucking in of 
the supraclavicular and the intercostal spaces may occur. The 
musculature of the chest is generally wasted 
and flabby, in keeping with the other marks 
of senility shown by the patient. 

The Rachitic Thorax. — In rickets the 
causes of the chest deformity are threefold: 
direct muscular action upon the soft bony 
structures, pressure upon these parts by the 
enlarged viscera, and the influence of atmos- 
pheric pressure. These combined factors 
tend to produce lateral compression, with 
relative increase in the anteroposterior diam- 
eter of the thorax, and to favor the formation of various local 
flattenings, prominences, depressions, and lineal markings upon its 




Fig. 29. — Transverse 
section of an emphysem- 
atous thorax. 



84 



PHYSICAL DIAGNOSIS 



surface. Fig. 31 illustrates a cross-section of a common type of 
rachitic chest. 

The most distinctive single sign of rickets is the so-called rachitic 
rosary , which consists of a beaded line paralleling each sternal border 




Fig. 30.' — The rachitic thorax (Jefferson Hospital). 



and corresponding to the course of the chondrosternal articulations. 
This double line of prominences, due to thickening of the costal 
cartilages, is to be felt in almost every rickety child, and in advanced 
cases it is also clearly recognizable on inspection. Another important 
sign of rickets, and one scarcely less "characteristic than the rosary, 
is an apparent shortening of the clavicles, with a marked exaggeration 
of their curves. Prominence of the thoracic spine (kyphosis) is a 
familiar type of vertebral deformity, and 
frequently the vertebral column is. bent for- 
ward (lordosis) and twisted laterally (sco- 
liosis) (Fig. 32). In some cases the spine 
remains flexible, but in others it is found 
to be fixed and rigid. The vertebrae may 
or may not be thickened, and sometimes they 
are studded with sharply pointed, conspicuous 
spinous processes. 
The pigeon-breast (chicken -breast; pectus carinatum; keel 
breast) is a common type of deformity met with in advanced rickets 
(Fig. 33). The anteroposterior diameter of the chest is unduly 
increased, the lateral thoracic walls are compressed, the sternum is 
pushed forward so that it projects like the keel of a ship, owing to 




Fig. 31, — Transverse 
section of a rachitic 
thorax. 



EXAMINATION OF THE THORAX 8$ 

the stress upon the flexible chondrosternal joints (Fig. 34). The 




Fig. 32. — Thoracic deformity due to spinal curvature (Jefferson Hospital). 

lower margins of the ribs are often distended or flared outward, partly 
by the intra-abdominal pressure exerted by such factors as ascites, 
tympanites, and enlarged liver and spleen, and 
partly by the traction of the diaphragm. A 
transverse groove, or furrow, extending from 
either side of the ensiform Cartilage and curv- 
ing downward and outward toward the axillae 
is also found in most cases of rickets; this 
furrow corresponds approximately to the in- 
sertion of the diaphragm, and is known as 
Harrison 1 s sulcus or furrow. 

The funnel-breast (Trichterbrust ; pectus excavatum) is also 
sometimes found in rickets, especially when adenoid and tonsillar 




Fig- 33 . — Transverse 
section of a pigeon- 
breast. 



86 PHYSICAL DIAGNOSIS 

hypertrophies coexist. It is characterized by a depression of the 
lower part of the sternum, extending from the tip of the xiphoid, 
perhaps as high as the middle of the gladiolus. This deformity is 
not essentially rachitic, for it may be congenital, secondary to non- 
rachitic diseases, or acquired as the result of pressure upon the lower 
sternum. The funnel-breast of the cobbler (Schusterbrust), due to 
constant pressure of the last against the lower part of the sternum, 




Fig. 34- — The pigeon-breast (Jefferson Hospital). 

shows a concavity limited to the lower gladiolus and to the 
ensiform, if not to the latter process alone (Fig. 35). 

The Flat Thorax. — This type of thorax is shallow and 
broad, although the length is not abnormally increased. It 
is distinguished chiefly by the conspicuous flatness and breadth 
of the anterior chest-wall and by the absence of the normal 



EXAMINATION OF THE THORAX 



87 



forward curve of the ribs, but the structural peculiarities of 
the phthisical thorax, noted above, are lacking. To be flat- 
chested does not necessarily condemn one to phthisis, but it is 
at least suggestive of a predisposition to this disease. 

The Fusiform Thorax. — Habitual tight lacing narrows and 
elongates the thorax, immobilizes the lower ribs, and contracts 
their intercostal spaces. In consequence of this compression 




Fig- 35- — Funnel-breast, due to the pressure of a cobbler's last (Philadelphia General 

Hospital). 



of the lower thorax the chest loses its normal conic shape, 
and is molded into a more or less fusiform or spindle-shaped 
structure, the waist-line decreases in circumference, and is low- 
ered at the expense of the flanks, the vertical extent of which 
is considerably lessened. Exaggerated upper thoracic breath- 
ing, upward displacement of the thoracic organs, ptosis of the 
abdominal viscera, and atrophy of the spinal muscles are the 
principal structural changes which, in the extreme instance, may 
result. 



88 PHYSICAL DIAGNOSIS 

The Boat-shaped Thorax. — In syringomyelia there may be 
noted a median depression of the upper anterior wall of the 
thorax, extending as far downward as the level of the fifth 
rib. The chest, hollowed out in this manner, has been termed 
the " thorax en bateau " by Marie, from its rude resemblance to 
a boat. 

The Thorax of Progressive Muscular Atrophy. — In the adult 
this myopathy may account for a most singular deformity, the thorax 
being converted into a roughly box-shaped structure whose per- 
pendicular walls project some distance beyond the surface of the 
flanks, which are immoderately concave. The waist, having an 
atrophied musculature, contrasts strikingly with the contour of the 
chest, and appears abnormally constricted and slender — the "taille 
de guepe" ("wasp waist") of Landouzy and other French writers. 
Other hall-marks of this type of thorax are loss of the normal curve 
of the chest-walls, extraordinary obliquity of the ribs, especially at 
the base, where their course is almost vertical, and general wasting 
of the thoracic muscles. 

The Gutter-chest. — As the result of antenatal and postnatal 
developmental defects the chest may be disfigured by the presence of 
a narrow, shallow, vertical gutter or groove corresponding to the 
median line of the sternum. This peculiarity, dubbed the "thorax 
en gouttiere" (Fere; Schmidt), is due to an exaggerated forward 
convexity of the costal cartilages, owing to which their sternal extrem- 
ities are closely approximated and the sternum pressed backward 
so as to form a narrow longitudinal median furrow. 

LOCAL ASYMMETRY OF THE THORAX 

Aside from the foregoing bilateral thoracic deformities, there are 
various defects of contour that may affect either one entire side or 
a circumscribed area of the chest. The anomalies due to lesions 
of the thorax and of the upper abdomen, described in the four groups 
given below, are to be distinguished from those secondary to disease 
of the spine, the consideration of which belongs to the subject of 
orthopedic surgery. 

Unilateral Bulging (Fig. 36).— Enlargement of one side of the 
thorax generally produces a leveling or a bulging of the intercostal 
spaces on the affected side; indeed, this obliteration of the inter- 
spaces may exist alone, and, if so, carries practically the same sig- 
nificance as an actual overdistention of the chest. Fig. 3.7 shows 



EXAMINATION OF THE THORAX 89 

the outline of this type of thoracic deformity. One-sided distention 
is met with in large pleural effusions, in pneumothorax, in neoplasms 




Fig. 36. — Unilateral enlargement of the thorax (Jefferson Hospital). 

of the lung and the pleura, and in compensatory emphysema of the 
lungs secondary to lesions of the opposite side. If due to this last 



Fig. 37. — Transverse section of a unilaterally enlarged thorax. 

cause, the contrast between the two halves of the chest is espe- 



90 PHYSICAL DIAGNOSIS 

daily striking, for here the emphysematous distention is brought 
into comparison, not with a normal opposite side, but with a 
shrunken, diseased one. 

Unilateral Contraction (Fig. 38). — Unilateral flattening or 
contraction of the chest, if extensive, causes lowering of the 




Fig. 38. — Unilateral retraction of the thorax due to empyema (Jefferson Hospital). 

shoulder and narrowing of the intercostal spaces on the affected 
side, together with more or less spinal curvature and twisting 
in. this direction. The contracted side is smaller than normal, 
while the opposite side is often found to be vicariously enlarged 



Fig. 39. — Transverse section of a unilaterally retracted thorax. 

(Fig. 39). Chronic pulmonary tuberculosis, interstitial pneu- 
monia, wide-spread pleural adhesions, and chronic compression 
of the lung by pleural effusions are the most important factors 
of this sort of deformity. In rare instances unilateral contrac- 
tion of the thorax may arise from pulmonary collapse due to the 
obstruction of a main bronchus by a tumor or by a foreign body. 



EXAMINATION OF THE THORAX 



9 1 



Circumscribed Prominences. — Local swellings or prominences 
upon the chest-wall, attributable to a wide range of causes, are 
seen most commonly upon the anterior surface, but they are by no 
means restricted to this part of the thorax. Bulging in the cardiac 
region (Fig. 40) may mean enlargement of the heart, pericardial 
effusion, pneumopericardium, or forward dislocation of the heart 
by the pressure of an aneurism or a new-growth. It is in young 
children that bulging of this part of the chest is most frequent and 
most noticeable. Aneurism of the aortic arch, by a process of ero- 
sion, may push through the overlying structures and, in course of 
time, cause a local tumor, simulated, at least superficially, by an 



/ 



1 




Fig. 40. — Precordial bulging due to cardiac 
hypertrophy (Jefferson Hospital). 



Fig 4i. — Sternal bulging due to aneurism 
of the aortic arch (Jefferson Hospital). 



abscess of the soft parts or by the simple irregularity in the contour 
of the sternal or the costochondral surfaces (Fig. 41). It is also 
possible, at first glance, to mistake an aneurism of the descending 
aorta for a left lateral twist of the spinal column. By pressure, a 
greatly enlarged liver may produce decided distention of the lower 
right thorax, while a splenic tumor may similarly bulge the left side 



9 2 



PHYSICAL DIAGNOSIS 



(Fig. 42). Hypertrophy of the breast in a male adolescent (Fig. 43) 
is a curious anomaly sometimes encountered. As already noted, 
the clavicles and the scapulae stand out prominently in the phthisical 
thorax. Prominence of either scapula may be caused by a scoliosis 
and by paralysis of the serratus magnus muscle, while the left scapula 
may be tilted outward by the backward erosion of a large aneurismal 
dilatation of the descending thoracic aorta. Tumors of the chest- 
wall, the lungs, and the pleura, empyema necessitatis, pulsating 
pleurisy, tuberculous disease of the bony thorax, mediastinal and 
subphrenic abscesses, and, rarely, hernia of the lung, are also cap- 
able of pushing out the chest-wall within a restricted area. An 
encysted pleural effusion, while it causes no local bulging, may 
obliterate the intercostal spaces over its site. Myxedema may account 





Fig. 42. — Thoracic and abdom- 
inal enlargement due to splenic 
tumor (Jefferson Hospital). 



Fig. 43- — Hypertrophy of the left breast in 
a male adolescent (Jefferson Hospital). 



for supraclavicular fibrofatty deposits — Verneuil's pseudolipomata. 
Subcutaneous emphysema is recognized as a. gaseous, crackling swell- 
ing which tends to disappear by absorption, and which is secondary 
to the rupture of some air-containing organ, or to a penetrating 
wound. 

Local Depressions. — The principal intrathoracic factors of local 
depressed and flat areas upon the surface of the thorax are apical 



EXAMINATION OF THE THORAX 



93 



tuberculosis, circumscribed pleural adhesions, and superficially 
seated pulmonary cavities. (See Figs. 24, 45, 46.) Among other 




Fig. 44. — Lateral compression of the Fig. 45. — Local retraction of the thorax due 
thorax {Jefferson Hospital). to pulmonary fibrosis and pleurisy (Jefferson 

Hospital). 

causes of such deformities may be mentioned atelectasis, bronchiec- 
tasis, fractured ribs, cicatrices consequent to rib resection and to 




Fig. 46. — Transverse section of a locally retracted thorax. 



healed empyema necessitatis, and atrophy or removal of a breast 
or of the musculature of the chest-wall. 



9 4 PHYSICAL DIAGNOSIS 

RESPIRATORY MOVEMENTS OF THE THORAX 

The student must become familiar not only with normal respiratory 
movements of the chest, but also with the abnormalities of breathing 
symptomatic of pathologic conditions. This information is acquired 
by observing the frequency, the rhythm, and the type of the thoracic 
movements, the degree and character of the chest expansion, and the 
extent and freedom of the diaphragm excursion. The adequacy of 
blood oxygenation, as shown by the color of the patient, is an inti- 
mate correlative of these signs, with which it will be considered 
below. 

Normal Respiratory Movements.— The respiratory cycle con- 
sists of an active inspiratory effort and a passive expiratory phase, 
followed by a pause, the relative duration of the two movements 
being thus expressed : inspiration : expiration : : 5 : 6. The respira- 
tory-pulse ratio averages about 1:4. In adults the normal respiratory 
jrequency is from 16 to 24 to the minute (Hutchinson) , while in children 
the average ranges from 44 in the new-born to 26 in the five-year-old 
child (Quetelet). Normal breathing is usually regular and quiet, 
but its rhythm and tranquillity may be deranged by mental disturb- 
ances, by muscular exertion, and by fatigue. The respirations may 
be timed either by simply watching the chest movements or by pal- 
pation, with the hand applied to the lower part of the thorax. 

The movements of the two sides of the chest are synchronous, and, 
except for a trifling physiologic overfulness of the right half, prac- 
tically symmetric. 1 Each inspiration increases all the diameters of 
the chest, and is attended by ascent and forward projection of the 
sternum, by ascent and eversion of the ribs, and by bulging of the 
upper epigastrium; with expiration the decrease in the chest diameters 
is accompanied by retrocession of the parietes and by reappearance 
of the normal epigastric hollow. The movements of inspiration 
are performed ordinarily by the diaphragm, intercostals, scaleni, 
serrati postici, and levatores costarum; but extraordinary efforts in 
breathing call into play the following accessory muscles : pectorales, 
quadratus lumborum, serratus magnus, sternomastoid, latissimus 
dorsi, infrahyoid, and erector spinas (Cunningham). The move- 
ments of expiration are due principally to the elasticity of the lungs, 
the ascent of the diaphragm, the weight of the chest-wall, and, in 
difficult, forceful deflation of the lungs, to the auxiliary action of the 
intercostal, triangularis sterni, and upper abdominal muscles. 

1 Most women, according to Ransome j show a greater respiratory movement 
of the left side of the chest. 



EXAMINATION OF THE THORAX 95 

The type of respiration differs normally in the two sexes, and is also 
influenced by the age of the individual. Thus, in women costal or 
thoracic breathing is the rule, which means that respiration is carried 
on chiefly by the upper part of the thorax, the scaleni and the upper 
intercostals being actively brought into play and the sternum and 
upper ribs conspicuously elevated and projected, while the epigas- 
trium remains immobile, or, at the most, moves but moderately. 
In men and in children of both sexes, on the contrary, respiration 
is of the abdominal or diaphragmatic type, being performed mainly 
by the action of the lower part of the thorax and of the diaphragm, 
whose descent causes bulging of the epigastrium during inspiration. 




Fig. 47. — Technic of determining Litten's diaphragm sign. 

In women of advanced age, whose chests have become rigid and 
fixed, more or less tendency toward abdominal respiration is also seen. 
The Diaphragm Phenomenon. — The normal inspiratory descent 
of the diaphragm is recognized as a faint, although perfectly apprecia- 
ble, shadow which travels vertically down the lower axilla during each 
full inflation of the lungs, from the sixth to the eighth or ninth inter- 
costal spaces. This so-called diaphragm phenomenon {Litterts sign) 
is shown most distinctly by placing the subject in dorsal decubitus, 
with the feet toward a window and the arms extended above the 
head, the observer standing behind or at the side of the bed, in the 
position indicated by the accompanying picture (Fig. 47). The 
shadow, which ordinarily has a vertical course of three or four inches 



9 6 



PHYSICAL DIAGNOSIS 



with each deep inspiration, is explained by the inspiratory separation 
of the diaphragm from the thoracic wall, an act that increases the 
extent of the complementary pleural sinus and exerts suction upon 
the intercostal spaces below the inferior border of the lung. 
Naturally, the diaphragm shadow is virtually imperceptible during 
expiration. 

Litten's sign is present in practically every healthy individual, 
except in those who are overmuscular or overfat, and it shows that 
the excursions of the diaphragm, the lung, and the pleura are unre- 
stricted. Conditions interfering with such movements partly or 
entirely abolish the diaphragm shadow upon the affected side, as is 
the case in pleural adhesion and effusion, basal pneumonia, extensive 
emphysema, pneumothorax, and neoplasms of the lower part of the 
thoracic cavity. To some extent subdiaphragmatic abscess, enlarge- 
ment of the liver and of the spleen, and extreme distention of the 
abdomen by fluid, gas, or solid tumors act in a similar manner, while 
in many cases of incipient phthisis the shadow is more or less inde- 
finable. In paralysis of the diaphragm the phenomenon is totally 
abolished, and in persons whose chest expansion is restricted the 
sign is difficult of detection. The presence of edema of the chest- 
wall effectually obscures the phrenic shadow. * 

Respiratory Alterations of the Subcostal Angle. — The study of 
the diaphragm shadow should always be supplemented by de- 
termining the presence of any unnatural change in the subcostal 
angle, as shown by Hoover's method of combined inspection and 
bimanual palpation with the thumbs symmetrically placed along 
the costal borders to serve as indicators of their divergence from, 
or convergence toward, the median line. This simple maneuver 
shows that with an identical limitation of inspiratory excursions, 
in both basal pneumonia and in pleural effusion, there is diverg- 
ence of the costal borders in the former and convergence in the 
latter. In pleural adhesion simple restriction is the rule, without 
definite change in the subcostal angle. Inspiratory divergence, 
with consequent widening of the subcostal angle, is observed in 
paralysis of the diaphragm, in subphrenic abscess, and in hepatic 
enlargement, while in emphysema, in pneumothorax, and in large- 
sized pericardial effusion the reverse occurs. In the foregoing the 
respiratory changes noted correspond to the affected side. Cardiac 
enlargements may alter the respiratory excursion of either the left 
costal margin or of both borders, the left being affected in left- 
sided enlargements, and both, with symmetric narrowing of the 
subcostal angle, in an enlargement in the median line, as commonly 
occurs in mitral stenosis. 



EXAMINATION OF THE THORAX 97 

Unlike Litten's diaphragm phenomenon, the movements of the 
costal borders are not obscured by either a thick layer of fat or 
by muscular overdevelopment of the subject, and, therefore, their 
study deserves wide clinical application in the differentiation of 
lesions of the lower thorax and of the upper abdomen. 

ANOMALIES OF RESPIRATION 

Under this caption are included the various disturbances of the 
respiratory excursion distinguished chiefly by deviations from its 
normal extent, frequency, and rhythm. 

Reversal of the Respiratory Type. — Costal breathing in a man 
and abdominal breathing in a woman, being just the reverse of the 
respiratory type normally occurring in the two sexes, are to be regarded 
as distinctly anomalous. Exaggeration of the type of breathing 
peculiar to either sex is to be interpreted in the same light. 

Costal breathing is associated with conditions that restrict the 
movements of the diaphragm, such as diaphragmatic pleurisy and 
paralysis, extensive pericardial effusion, emphysema, ascites, tympan- 
ites, abdominal tumor, and peritonitis. Exaggeration of the respir- 
atory movements of the upper thorax attends various forms of dyspnea, 
notably those of hysteric origin. 

Abdominal breathing, prevailing because of some mechanical im- 
pediment to the free movements of the chest, occurs in bilateral 
pleural effusion, in massive pneumonia, in calcareous disease of 
the chest-wall, and in scleroderma. Spinal paralysis, tetanus, and 
strychnin poisoning also throw the work of the thoracic movements 
upon the abdomen. The conditions noted below as factors of 
deficient expansion, owing to the painful breathing they excite, also 
favor more or less the abdominal type of respiration. 

Sternomastoid Breathing. — Undue contraction of the sternomastoid 
muscles is noticeable whenever the respiratory function suffers any 
extraordinary stress, and, therefore, such action is a common sign 
in most forms of dyspnea (q. v.) . So conspicuous are the contrac- 
tions of this muscular group in the dying state that this action has 
been termed a " veritable death's call" (R. H. Chase). 

Alterations in the Degree of Expansion. — A general defi- 
ciency in the expansion of the chest, or shallow breathing, may be 
simply a personal peculiarity, and hence is without definite import; 
more often, however, it is suggestive of either latent or active pul- 
monary tuberculosis, especially if flat-chestedness coexists. Feeble 
expansion is perhaps best illustrated by the thoracic immobility 



9 8 



PHYSICAL DIAGNOSIS 



incident to such conditions as collapse, acute syncope, trance, and 
the adynamia of acute febrile diseases. The overdistended thorax 
of the emphysematous subject can expand but slightly, and the 
mobility of the chest is impaired by laryngeal or tracheal stricture, 
and by paralysis or spasm of the respiratory muscles and of the 
diaphragm. Deficient chest expansion from ossification of the costal 
cartilages (Bryson's sign) often occurs in Graves' disease. Painful 
breathing limits the respiratory excursion, which is restricted for 
this reason in pleurisy, pericarditis, peritonitis, intercostal neuralgia, 
rheumatism, and diseases of the chest-wall. 

Wavy and uneven expansion, or a peculiar undulatory type of 
respiratory movements, frequently develops during the adynamia of 
the so-called " typhoid state." 

Deficient expansion and inspiratory retraction of the interspaces 
sometimes coexist, as in stenosis of the upper air-passages and in 
diffuse bronchopneumonia, in which conditions inflation of the lungs 
is performed with great difficulty. Retraction of the lower inter- 
spaces with a simultaneous bulging in the supraclavicular regions 
is a distinctive finding in advanced emphysema. Bronchial stenosis, 
atelectasis, and pleural adhesion are factors of unilateral, and of 
limited, circumscribed intercostal retraction. 

Unsymmetric expansion, characterized by a one-sided deficiency 
of the respiratory movements, is commonly met with in conditions 
that mechanically interfere with the movements of the affected lung — 
pleural effusion, wide-spread pleural adhesion, massive pneumonia, 
pneumothorax, and tumor of the lung; while a lung crippled by 
tuberculosis, by cirrhosis, or by atelectasis also fails to inflate and 
deflate normally. Either a foreign body lodged in a main bronchus 
or a tumor constricting its lumen can account for unilateral interfer- 
ence with expansion on the side implicated. Right-sided restriction 
of breathing may be symptomatic of hepatic enlargement, and left- 
sided, of hypertrophied spleen. 

Circumscribed deficiency of expansion, showing as a local patch of 
immobility upon the chest-wall, is significant of some limited lesion 
of the lung, pleura, or pleuropericardium. Immobility and lagging 
in an infraclavicular space suggests tuberculosis, pneumonia, or 
adhesive pleurisy in this region; if it affects the lower part of the 
thorax, basal pneumonia or diaphragmatic pleurisy is to be thought 
of; and if it be localized in the region of the heart, pericardial adhe- 
sions are to be suspected. 

A general increase in the expansion of the chest occurs as the physio- 
logic effect of hard exercise, attends various emotional states, and is 



EXAMINATION OF THE THORAX 99 

seen in certain forms of dyspnea. The vicarious overaction of one 
lung or of a part of one lung is the underlying cause of a unilateral 
or circumscribed increase in expansion. 

Alterations in the Frequency of the Respiratory Movements. — 
Simple rapid breathing, or polypnea, usually attended by shallowness 
of the respiratory excursion, occurs normally in young children, and 
is the physiologic result of active exercise, although in the latter 
instance the breathing is deep, as well as rapid. Accelerated respira- 
tion is also met with in neurotics, in many of the acute fevers, and in 
pulmonary lesions, such as pneumonia and tuberculosis, which not 
only diminish the aerating surface of the lungs, but also elaborate 
toxins that probably stimulate the respiratory center. 

Slow breathing, or oligopnea, occurs in many conditions of coma, 
collapse, and shock from various causes; in cerebral tumor, apoplexy, 
and meningitis; in poisoning by opium, chloral, chloroform, aconite, 
and antimony; and, occasionally, in bronchial asthma. The associa- 
tion of arythmic and difficult respiration is discussed under Dyspnea 
(q. v.). ^ 

Respiratory Arhythmia. — Simple irregularity, often temporary, 
in the rhythm of the respiratory movements is not necessarily patho- 
logic, since it is often referable to trivial psychic disturbances. It is, 
on the contrary, a sign of grave import in apoplexy, uremia, menin- 
gitis, cerebral tumor, lesions of the medulla, and in states of collapse. 
Respiratory arhythmia may also accompany chorea, and frequently 
is found in pneumonia and in atelectasis, being evidenced in these 
last two conditions as a distinct post-inspiratory pause. 

Jerky respiration, characterized by a series of spasmodic interrup- 
tions of inspiration and expiration, is in some instances purely hysteric, 
but in others it is attributable to some one of the factors of restricted 
respiration referred to in a preceding paragraph. (See p. 97.) 
Chorea, asthma, hemiplegia, and rabies are additional causes of this 
respiratory peculiarity. 

Cheyne-Stokes respiration is characterized by periodic disturbances 
of the respiratory rate, rhythm, and volume, alternating with intervals 
during which breathing entirely ceases, these two contrasting phases 
recurring in regular cycles. Thus, one of these quiescent intervals 
(period of apnea) is followed by slow and shallow respirations, which 
progressively increase in both frequency and in volume until they 
reach an acme (period of dyspnea) , after which they gradually become 
slower and shallower until, having ceased entirely, another quiescent 
period begins (Fig. 48). The length of the two periods is variable — 
a few seconds to one or even two minutes for the dyspneic phase, 
and as long as one minute for the apneic. Sighing and snoring 



IOO 



PHYSICAL DIAGNOSIS 



sometimes attend the deep respiratory efforts just preceding the 
acme of dyspnea, and cyanosis is a familiar objective symptom 
at this time. The difference between Cheyne-Stokes, normal, and 




Fig. 48. — Cheyne-Stokes respiration; upstroke: inspiration; downstroke: expira- 
tion. The small waves in the period of apnea are due to the heart-beat (Pneumo- 
gram by Dr. G. Bachmann). 

shallow respiration is graphically shown by Fig. 49. It is of some 
importance to recall Eyster's observation, that arterial hyperten- 
sion accompanies the dyspneic period of Cheyne-Stokes respiration 
due to cerebral compression, wliile in that due to cardiorenal dis- 



Normal 



A/WWWWWV 



Shallow 



Cheyne- 
Stokes 




Fig. 49.— Normal and pathologic types of respiration. 



ease and other factors the blood-pressure rises during the apneic 
stage. As a rule, the pulse-rate appreciably shows during apnea, 
but in some cases the reverse occurs. 

The persistence of Cheyne-Stokes respiration ranges from a few 
hours to as long as several weeks, or, in the extreme case, several 
months. The patient sometimes becomes insensible during the 
phase of apnea, but regains consciousness as breathing is resumed. 



EXAMINATION OF THE THORAX IOI 

This type of respiration also may occur in coma, as well as in 
ordinary sleep. 

Cheyne-Stokes respiration invariably has a grave, although not 
necessarily a fatal, significance. It may attend almost any pro- 
foundly comatose state, but its presence especially suggests factors 
such as apoplexy, cerebral tumor or softening, meningitis, uremia, 
diabetes mellitus, opium-poisoning, and fatty heart or other degen- 
erative cardiac lesions. With less frequency it is observed in the 
typhoid states of various acute infectious diseases, in general paral- 
ysis, and as the result of embolism and of hemorrhage. Cheyne- 
Stokes ; respiration is due to diminished irritability of the respira- 
tory center, but whether this can be accounted for simply by 
fatigue (Rosenbach's belief) or by faulty oxygenation (Traube's 
view) is a moot point. 

Meningeal respiration consists of recurring periods of apnea, 
ranging from five or ten to twenty or thirty seconds' duration, and 
separated by intervals marked by irregularity of rhythm and of 
force. The apneic periods recur irregularly, and commonly are 
preceded or succeeded by a deep sighing respiration. This res- 
piratory anomaly, also known as Biotfs respiration, is particularly 
suggestive of meningitis, but it may be symptomatic of the same 
factors to which typical Cheyne-Stokes respiration is referable. 

An extraordinary example of voluntary apnea in a young athlete, 
who held his breath for ten minutes and ten seconds, is recorded 
by Saxton Pope. 

Stertorous respiration, or snoring, caused by the vibrations of 
a relaxed soft palate, occurs usually, but not exclusively, during 
either sleep or coma. It is a well-known sign of profound sleep in 
many healthy persons who sleep with their mouth open, and is heard 
with great constancy in the condition known as "mouth-breathing," 
consequent to tonsillar hypertrophy, postnasal adenoids, quinsy, 
and postpharyngeal abscess, the noisy snoring of this last- 
named condition having been dubbed the " hen-cluck " stertor. Of 
the more serious factors of stertorous breathing, one should remember 
paralysis of the soft palate, and the comatose states of uremia, apo- 
plexy, diabetes mellitus, asphyxia, opium-poisoning, pulmonary 
edema, epilepsy, and cerebral compression. 

Stridulous respiration, denoting stenosis of the larynx or trachea, 
is audible, especially during inspiration, as a medley of harsh, hissing, 
or whistling vibratory sounds, the production of which is due to some 
local lesion of the parts or to a primary interference with the functions 
oi the laryngeal muscles. Thus, stridor is commonly the result of 
inflammatory turgescence, edema, diphtheria, neoplasm, and of a 



io2 PHYSICAL DIAGNOSIS 

foreign body in the larynx or trachea. Or it may relate to the laryn- 
geal spasm of spasmodic croup, laryngismus stridulus (child-crowing; 
thymic asthma), locomotor ataxia (laryngeal crisis), tetanus, or 
strychnin-poisoning. In other instances irritation of the inferior 
laryngeal nerve by the encroachment of an aneurism, a neoplasm 
of the mediastinum or trachea, a mass of enlarged bronchial glands, 
or a dislocated heart is the exciting cause of stridor. Respiration 
through a tracheotomy tube produces a rasping sound not unlike 
that made by filing the teeth of a saw — hence the term, stridor 
serraticus. The stridor of tracheal stenosis is also known as the 
"leopard's growl." 

The "asthmatoid wheeze" is described by Chevalier Jackson as a 
sign of foreign body in the larynx or bronchi. It is elicited by listen- 
ing in front of the open mouth of the subject, who meanwhile 
breathes regularly and deeply, the sign appearing at the end of 
forced expiration as a dry, harsh, asthmatic wheeze, uninfluenced 
by coughing, but affected by postural changes. 

DYSPNEA 

Dyspnea means difficult or labored respiration, and these laborious 
efforts to breathe are the distinctive hall-mark of the sign, irrespective 
of any coexisting disturbances of the respiratory rate, rhythm, and 
depth. When dyspnea is striking, the respiratory movements are 
obviously embarrassed, as shown by the overaction of the accessory 
muscles of respiration upon which demand is made, and the patient's 
anxious face, dilated pupils, moist skin, dry tongue and lips, gaping 
mouth, dilated alae nasi, and cyanosis constitute a very distinctive 
clinical picture of the extreme respiratory distress. When the 
dyspnea is so urgent that the subject can breathe only when in an 
upright position, the term orthopnea is used. 

Labored inspiration, with natural expiration, the effort here being 
made to inflate the lungs, is known as inspiratory dyspnea; but when, 
on the other hand, expiration is interfered with, the effort being made 
to deflate the lungs, the condition is one of expiratory dyspnea. When 
both inspiration and expiration are labored,— and this is, by far, 
the commonest type, — the term mixed dyspnea is employed. Accord- 
ing to the nature of the underlying factor or factors, dyspnea is either 
constant or paroxysmal. When the patient is conscious of shortness, 
of breath, subjective dyspnea exists; while in objective dyspnea the 
labored breathing is apparent to the examiner, although the patient 
is not necessarily distressed thereby. 

Types of Dyspnea.— Aside from the dyspnea arising from 
purely functional causes, the most important clinical types are those 






EXAMINATION OF THE THORAX 103 

attributable to anemia, toxemia, stenosis of the air-passages, and 
organic lesions of the lungs and the cardiovascular system. These 
causes, together with others of minor interest, may be considered 
briefly under the following headings. 

Functional Dyspnea. — Any form of active muscular exercise may 
be responsible for a temporary dyspnea of the mixed type, such as 
that illustrated by the labored, deep, and hurried breathing of the 
oarsman after a hard row, or of the sprinter after a hundred yards' 
dash. Temporary congestion of the pulmonary capillaries best 
accounts for this form of dyspnea, though it may be true that there 
is some irritation of the respiratory center by circulating toxins 
elaborated by abnormally active tissue metabolism. Trifling exer- 
tion, insufficient even to hurry the respiration of a normal person, is 
often sufficient to embarrass seriously the breathing of those affected 
with incipient phthisis, imperfectly compensated cardiac disease, 
chronic bronchitis, emphysema, anemia, and obesity. 

The functional neuroses account for a similar kind of dyspnea, as 
in persons of a nervous temperament, especially neurotic and hysteric 
women, whose shortness of breath is distressing enough to amount 
to an actual dyspnea, despite the fact that no more tangible cause 
than simple excitement or emotion is apparent. Perverted action 
of the respiratory center has been suggested as the explanation of the 
dyspnea in such cases. 

Anemic Dyspnea.— In high-grade anemia the diminished oxygen 
content of the blood leads to difficult breathing and to increased 
frequency and depth of the respiratory movements, in order thus to 
compensate for the oxygen deficiency by an unusually thorough oxy- 
genization of all the available hemoglobin. The degree of a purely 
anemic dyspnea stands in direct relation to the extent of the hemo- 
globin loss, being more decided in pernicious anemia, in chlorosis, 
and in acute leukemia than it is in the ordinary forms of secondary 
anemia. Here also may be mentioned the dyspnea due to the breath- 
ing of impure air, as illustrated by the form of respiratory distress 
know as " mountain sickness," caused by breathing air deficient in 
oxygen, and by the extreme dyspnea, if not the asphyxia, of coal-gas 
poisoning, in which carbon monoxid replaces the oxygen of the 
circulating blood. 

Toxemic Dyspnea. — In active fevers rapid, difficult breathing is 
likely to develop from the effect of the attendant toxemia, as well 
as from irritation of the respiratory center by abnormally warm 
blood. Uremic dyspnea, observed in the nephritides, may be a sign 
of uremic intoxication, but it also must be referred to such additional 
factors as cardiovascular disturbances and to inflammatory and me- 



I0 4 PHYSICAL DIAGNOSIS 

chanical implication of the bronchopulmonary apparatus. In gen- 
eral, the uremia of renal disease is the evidence of an attempt of the 
lungs to compensate the existing acidosis, and to a less extent it is 
a sign of increased excitability of the respiratory center. So-called 
"renal asthma" is an unfortunate term, generally confounded with 
the breathlessness of nephritis, though it must be admitted that an 
occasional instance of true bronchial asthma is possibly of uremic 
origin. Renal dyspnea is frequently paroxysmal, but it may be of 
a continuous type, with or without Cheyne-Stokes breathing and 
cyanosis. Diabetic dyspnea, or Kussmaul's air-hunger, is commonly 
of the mixed type, and is characterized by deep, but not unduly 
rapid, respiratory excursions, with or without cyanosis. It frequently 
ushers in an attack of diabetic coma during which it may become 
transformed into Cheyne-Stokes respiration. This precomatose 
form of dyspnea is explained partly by the toxic action of the diabetic 
acidosis and partly by the fact that the oxygen capacity of diabetic 
blood is subnormaL Toxemia plus hemolytic reduction of the oxy- 
gen content of the blood is the credible factor of the dyspnea incident 
to malignant jaundice, hepatic cirrhosis, insolation, and the malarial 
chill. 

Obstructive and Mechanical Dyspnea. — It is convenient here 
to consider the varieties of respiratory difficulty symptomatic of 
stenosis of the air-passages, of mechanical interference with the 
thoracic movements, and of spastic or paralytic lesions of the 
respiratory muscles. 

Stenosis of the upper air-passages, in that it obstructs the free 
entrance of air to the lungs, is a prominent cause of inspiratory 
dyspnea characterized by slow, deliberate, deep respiratory efforts, 
which tend to overcome the obstruction much more effectually than 
does hurried, shallow breathing. When the grade of stenosis is 
so extreme that the efforts of inflation actually rarefy the pulmonary 
air, inspiratory retraction of the lateral walls of the thorax and of the 
epigastrium is noticeable, and the lower intercostal spaces, the supra- 
sternal notch, and the supraclavicular regions are sucked in with 
each deep breath. Stridor, as noted in a foregoing paragraph, is 
also a noteworthy sign of stenosis of the upper air-passages. Of 
the conditions responsible for respiratory stenosis, the following 
are important: tonsillar enlargement and retropharyngeal abscess; 
membranous, edematous, and inflammatorv occlusion of the larynx; 
laryngismus stridulus, croup, and paralysis of the dilators of the 
glottis; and stenosis of the larynx, trachea, or main bronchus 
by cicatrix, foreign body, neoplasm, glandular enlargement, or 
aneurism. In young children alarming paroxysms of dyspnea 



EXAMINATION OF THE THORAX 105 

and respiratory stridor may be excited by the pressure of a thymus 
hyperplasia upon the trachea. 

In extreme bronchial obstruction there is wide-spread blocking of 
the bronchioles by swelling, spasm, or exudate, and in consequence 
rapid breathing and urgent expiratory dyspnea occur, marked by great 
prolongation of expiration, cyanosis, and perhaps by stridor. This 
is especially prone to occur in the diffuse catarrhal pneumonia of 
young children, in bronchial asthma, and in fibrinous bronchitis of 
the smaller tubes. 

Mechanical restriction oj the thoracic movements provokes dyspnea, 
commonly of the mixed type, attended by accelerated breathing, 
and by compensatory overaction of the unaffected side, in unilateral 
interferences. The causes underlying this variety of dyspnea are 
practically those of deficient expansion (q. v.), namely: conditions 
provocative of painful breathing; rigidity and deformity of the bony 
thorax; intrathoracic tumor and paralysis of the respiratory muscles; 
pleural collections of gas or fluid; and upward displacement of the 
diaphragm by enlarged abdominal viscera, tumor, meteorisrri, or 
ascites. 

Pulmonary Dyspnea. — Diminution of the respiratory surface, 
due to diseases of the pulmonary parenchyma, is attended by dysp- 
nea and rapid breathing, the degrees of which are determined chiefly 
by the extent to which pulmonary ventilation is crippled. In some 
instances the attendant toxemia is also actively concerned, and in 
others some of the additional factors of dyspnea enumerated above 
are partly responsible. Pulmonary dyspnea may be met with in any 
form of consolidation, collapse, or distention of the lungs, of which 
good examples are furnished by croupous pneumonia, tuberculosis, 
edema, infarction, fibrosis, and neoplasm; by atelectasis due to 
catarrhal pneumonia and to pericardial or pleural effusion; and by 
the overinflation of the vesicles in hypertrophic emphysema. In 
the last-named disease a highly distinctive expiratory dyspnea pre- 
vails; in most of the others there is difficulty with both inspiration 
and expiration. 

Cardiac Dyspnea. — The dyspnea of uncompensated cardiac dis- 
ease depends upon general circulatory stasis, by fault of which the 
system is overcharged with venous blood, the oxygen tension being 
lowered with a consequent increased stimulation of the respira- 
tory center. Owing to this defect, the lungs become rigidly fixed 
in the position of extreme inspiration, on account of the great 
overdistension of the pulmonary capillaries with blood. These 
two circumstances excite the rapid, shallow, arhythmic dyspnea 
which develops in various structural lesions of the heart, but 



106 PHYSICAL DIAGNOSIS 

especially in mitral disease, during the stage of broken compensa- 
tion. The associated bronchitis, with its abundant catarrhal secre- 
tion, aggravates the respiratory distress already existing. Sud- 
den, acute engorgement of the pulmonary capillaries gives rise to 
urgent dyspnea and cardiac irregularity — the condition mistermed 
" cardiac asthma," which is to be clearly distinguished from true 
bronchial asthma and from uremic dyspnea. 

CYANOSIS 

Cyanosis betrays a deficiency of oxygen and an excess of carbon 
dioxid in the capillary circulation, and is recognized as a dusky blue 
or even purple discoloration of the skin and the mucous membranes. 
This discoloration tends to show most decidedly in relatively trans- 
parent parts remote from the chest — the tips of the fingers and toes, 
the knees and ankles, and the lips, nose, cheeks, and ears. Cyanosis 
blended with pallor gives to the skin a livid hue, and combined with 
jaundice, an extraordinary greenish tint. 

The factors of general cyanosis relate to the faulty oxygenation of 
the blood in the lungs, and to any obstruction of the venous return 
flow productive of congestion within the veins. Like dyspnea, 
cyanosis may accompany disorders of the cardiovascular or respiratory 
system, capable of exciting the foregoing disturbances. Aside from 
such causes as these, cyanosis is symptomatic of vasomotor paralysis 
and of the methemoglobinemia consequent to poisoning by acetanilid 
or by nitrobenzol. Permanent cyanosis with splenomegaly and 
polycythemia constitutes the syndrome of Saundby and Russell, 
chronic cyanotic polycythemia. 

Local cyanosis is produced by either partial or complete oblitera- 
tion of. a venous trunk by thrombosis or by external pressure, in 
consequence of which blueness develops in the part distal to the 
constriction. 

VENOUS ENLARGEMENT AND TORTUOSITY 

Actual overfulness of the veins upon the surface of the thorax is to be 
distinguished from the conspicuous venous trunks so commonly 
observed in the thin-skinned blond and in those who are greatly 
emaciated. In a healthy person one occasionally meets with a general 
dilatation and even with an abnormal tortuosity of the cutaneous 
veins of the chest, a peculiarity best explained by ascribing it to a con- 
genital weakness of the venous walls. More often, however, venous 
enlargement is traceable to either a general or a local interference 
with the venous circulation, due, for instance, to right-sided cardiac 



EXAMINATION OF THE THORAX 107 

weakness, to thrombosis, and to mediastinal growths (Figs. 50 and 
51). The direction of the venous flow is determined by stroking the 
enlarged vein so as to empty the blood therein, and then noting the 
direction from which the collapsed vessel refills when the pressure 
is removed. Or the vein may be compressed with the finger-tip 
and the relation of the resulting turgescence to the point of con- 
striction observed (cf. p. S 2 Q- 

Enlarged mammary veins may arise from several different causes: 
they are not uncommon during the late stages of pregnancy and 
during lactation; they are also associated with many cases of malig- 
nant disease of the breasts; and they may betray an obstruction, by 




Fig. 50. — Venous tortuosity of the thoracic wall (Episcopal Hospital). 

the pressure of a thoracic aneurism or a new-growth, to the venous 
return of blood from the breasts. 

A ramification of small venules over the upper chest, with 
prominence of the jugulars, is sometimes found in tuberculous 
enlargement of the bronchial glands. Abnormal fulness of the 
superficial veins in the neighborhood of the sternum suggests medias- 
tinal tumor, of which such a sign is one of the early clinical manifesta- 
tions (Fig. 50) . The pressure of a tumor or of a cicatrix in the axilla 
may account for overdistention of the veins of the upper arm on the 



io8 



PHYSICAL DIAGNOSIS 



affected side (Fig. 52). A purplish fringe of dilated veins coursing 
symmetrically along the costal arch is a familiar finding in right ven- 
tricular dilatation, in atrophic cirrhosis of the liver, and in chronic 
adhesive pleurisy. In portal vein engorgement and obstruction 





Fig 51. — Venous engorgement of thoracic and abdominal walls (Jefferson Hospital). 

the greater part of the entire lower thorax is sometimes encroached 
upon by the upward extension of the dilated veins of the upper 
abdominal region. 

EDEMA OF THE THORACIC WALL 

This is easily detected by its tumid appearance and by the fact 
that the tissues pit upon pressure and retain temporarily the imprint of 
the finger. Local edema, perhaps with some discoloration, may be a 
sign of impending perforation in empyema necessitatis or of abscess 
of the parietes; but purulent pericarditis, mediastinal abscess, pul- 
monary hydatid, aneurism of the aortic arch, and angioneurotic 
edema must also be recalled as possible factors. Occlusion of the 



EXAMINATION OF THE THORAX 



IO9 




Fig. 5 2 - — Edema of the arm, due to lymphatic obstruction (Jefferson Hospital). 




Fig. 53. — Edema of the lower extremities (Jefferson Hospital). 



IIO 



PHYSICAL DIAGNOSIS 




Fig. 54. — Nephritic edema of the face (Jefferson Hospital). 




Fig- 55. — Cardiorenal anasarca (Jefferson Hospital). 



EXAMINATION OF THE THORAX 



III 



superior vena cava may account for persistent edema of the thorax, 
neck, and upper limbs, with cyanosis and compensatory dilatation 
of the superficial veins. General edema affecting the greater part 
of the surface of the chest, is referable to some form of anasarca, 
for the cause of which the heart, the liver, and the kidneys should 
be examined (Fig. 55). In this connection that form of congenital 
dropsy known as fetal erythroblastosis, a defective hemogenesis 
with anasarca and fluid in the body cavities, should be recalled. 

GLANDULAR ENLARGEMENT 

Routine examination of the neck and axilla should be made, in 
order to detect glandular swellings symptomatic of such lesions as 
simple adenitis, tuberculosis, syphilis, malignant tumors, benign 




Fig. 56.— Common sites of superficial glandular enlargements. 



lymphoma, leukemia, and Hodgkin's disease. The cervical glands, 
lying along and beneath the sternocleidomastoid muscle, are the 



112 PHYSICAL DIAGNOSIS 

favorite site of simple acute adenitis tending to end by resolution, 
and met with in the specific fevers of childhood and in local infec- 
tions of neighboring parts. Of the former class of factors, measles ? 
scarlatina, diphtheria, glandular fever, and pertussis are important 
examples; and of the latter group of causes, dental caries, stomatitis, 
tonsillitis, and otitis. The submaxillary glands are frequently the 
earliest site of tuberculous adenitis, which in the course of time tends 
to implicate the other lymphatics of the neck (Fig. 59). Scrofulous 
glands are prone to early softening, suppuration, and fistulation, 
and are often accompanied by definite signs of tuberculosis of the 
lungs and bronchial glands. These glands are also a favorite site for 




Fig. 57- — Benign tumor of the neck (Jefferson Hospital). 

the growth of a local benign lymphoma, a tumor of this type being 
strictly limited to a single group of glands, and forming a dense, 
painless swelling which does not caseate, suppurate, nor adhere to 
adjacent parts (Fig. 58). Vincent's angina, diphtheria, mumps, 
stomatitis, actinomycosis, and infections of the mouth and adjacent 
structures are among the other factors of submaxillary adenitis. 
The occipital glands are commonly enlarged in syphilis, being recog- 
nized as a group of painless, freely movable masses of cartilaginous 



EXAMINATION OF THE THORAX 



113 




Fig. 58. — Lymphoma of the cervical glands (Jefferson Hospital). 




Fig. 59. — Bilateral tuberculous enlargement of the cervical lymphatic glands 
R (Jefferson Hospital). 



U4 



PHYSICAL DIAGNOSIS 



hardness and moderate size. Whenever such masses are felt, the 
examiner should look for the initial lesion and search for inguinal 




k h --I 

Fig. 60. — Bilateral sarcomatous enlargement _ of the cervical lymphatic glands 
(Jefferson Hospital). 




Fig. 6v — Generalized glandular enlargement in Hodgkin's disease (Jefferson 

Hospital). 

adenitis and for supratrochlear kernels just above the internal 
condyle of the humerus. The posterior cervical, glands are pecu- 



EXAMINATION OF THE THORAX 



"5 



liarly susceptible to enlargement in rotheln, and the occipital 
glands are affected in irritation and inflammation of the scalp. 
Enlargement of the parotid gland, aside from mumps and neo- 
plasms, may be secondary to septicemia, pneumonia, enteric fever, 
and similar infections; to lesions of the abdomen and pelvis; and 
to facial paralysis. 




Fig. 62. — Cystic enlargement of the thyroid gland (Jefferson Hospital). 



Enlargements of the axillary glands (Fig. 61) may be secondary 
to vaccinia, infected wounds, general septicemia, and bubonic 
plague; they are part and parcel of the general glandular hyper- 
plasia of Hodgkin's disease and of leukemia; and, like many of 
the lymphatic chains heretofore mentioned, they are sometimes 
symptomatic of malignant tumors. The extensive glandular tu- 
mors of Hodgkin's disease and of leukemia are in nowise dis- 
tinctive, from a clinical standpoint, but the blood-report furnishes 
an easy means of differentiation : normal or but moderately anemic 
blood in the former, and either myelemia or lymphemia in the 
latter. A malignant neoplasm of the lymphatic structures, if 



IX 6 PHYSICAL DIAGNOSIS 

cancerous, is to be regarded as secondary to a primary growth 
in another situation— in the mouth, the upper air-passages, or 
the mediastinum, if the cervical lymphatics are implicated; in 
the breast, if the axillary glands are large. A sarcomatous gland- 




Fig. 63.— Subcutaneous nodules in a case of general sarcomatosis (Jefferson Hospital). 

ular swelling is likely to be fixed and immovable, and tends early 
to infiltrate, inflame, and ulcerate adjacent tissues. The soft parts 
about a lymphosarcoma may pit upon pressure, if, indeed, they 
do not seem abscessed, and the tumor is sometimes covered by a 
maze of tortuous, congested cutaneous veins. 

Enlargement of the lateral thoracic glands in the midaxilla is 
suggestive of tuberculosis, either pulmonary or bronchial. Zeb- 
rowski found this type of adenitis in 20 per cent, of all cases of 
phthisis, usually on the side of the affected lung. Other factors 
of enlarged glands in this site include simple hyperplasia, malig- 
nant neoplasms of the lung, pleura, mediastinum, liver and stom- 
ach, lymphatic leukemia, and Hanot's hepatic cirrhosis. 



EXAMINATION OF THE THORAX 



117 




Fig. 64. — Thyroid enlargement in Graves' disease (Jefferson Hospital). 




Fig. 65. — Thyroid enlargement in Graves' disease (without exophthalmos) -(Jefferson 

Hospital). 



n8 



PHYSICAL DIAGNOSIS 



Enlargement of the thyroid gland shows as a globular swelling, 
more often of irregular than of symmetric contour, situated between 
the larynx and the suprasternal notch, and intimately attached to 
the trachea, with which it moves during deglutition (Fig. 62). Such 
a tumor generally proves to be goitrous, either simple cystic or exoph- 
thalmic, the ordinary bronchocele being attended by no ill effects 
save perhaps those due to pressure, while in Graves' disease one 
expects to find three other cardinal signs — tachycardia, exophthalmos, 




Fig. 66.— Multiple fibroma (molluscum fibrosum) of the back (Philadelphia General 

Hospital). 

and tremor (Figs. 64 and 65). Less commonly the enlargement is 
due to acute thyroiditis, abscess, tuberculosis, neoplasm, or acro- 
megaly. Puberty in girls, menstruation, and pregnancy all may 
be accompanied by a moderate, transient swelling of the thyroid 



EXAMINATION OF THE THORAX Iig 

gland, excited by acute congestion. Myxedema, in the form of 
either cretinism or Gull's disease, is characterized by atrophy of the 
thyroid, and this also is true of the exceptional case of acromegaly. 

PAIN IN THE THORAX 

Pain in the chest may be symptomatic not only of diseases of the 
thorax and its contents, but also of lesions affecting more remote 
regions, such as the gastro-intestinal and the genito-urinary tracts, 
the peritoneum, the spine, and other parts of the nervous system. 
Such extrathoracic factors as these are to be recalled in deciding 
the origin of pains affecting the thorax. Of the many localized chest 
pains, those referred to the apex of the lung, the sternum, the breast, 
the precordia, the back, and the lower thoracic regions have, in many 
instances, more or less definite significance; but, as a rule, the various 
unclassified pains felt in other areas of the chest are most ambiguous 
clues (Fig. 67). 

Pain in the right shoulder is occasionally an accompaniment of 
aortitis and of aneurism of the innominate artery, but more often 
it is due to some disease of the liver or of the bile-ducts. Possible 
factors of pain in the left shoulder include diaphragmatic pleurisy, 
distention of the colon, gastritis, gastrectasis, duodenal ulcer, and 
suprarenal lesions. 

At the apex of the lung pain is commonly elicited in apical tuber- 
culosis, owing to the attendant pleurisy. 

Sternal pain may mean bronchitis, enlarged bronchial glands, or 
bronchial obstruction by a foreign body; aortitis, aortic valvulitis, 
aortic aneurism, or angina pectoris; and mediastinal inflammation, 
abscess, or tumor. Pain in this situation is also very common in 
gastric disorders, in syphilis, and in diseases of the bone itself. 

Pain in the precordia, which is quite as likely to be extracardiac 
as cardiac, has among its numerous factors functional and organic 
cardiac disease, aneurism of the aorta, angina pectoris, neuralgia, 
myalgia, vasomotor disturbances, and disorders of the medias- 
tinum, esophagus, stomach, and colon. Precordial pain directly 
referable to circulatory disturbances occurs in endocarditis, myo- 
carditis, pericarditis, cardiac syphilis, arteriosclerosis, tobacco 
heart, and hyper- and hypotensive myocardial insufficiency. 

Pain in the breast, aside from that due to diseases of the mammae, 
may be associated with menstruation, pregnancy, and lesions of the 
uterus and the ovaries. Pleural pains, as in the pleurisy of croupous 
pneumonia, are also ordinarily referred to this region. 

Pain in the right hypochondrium suggests especially diseases of the 



120 



PHYSICAL DIAGNOSIS 



liver and the bile-passages, malignant growths of the pancreas, the 
hepatic colon, or the duodenum, and aortic valve defects; in the 
left hypochondrium, pain may be due to diseases of the spleen, 
impaction of the splenic colon, inflammation, ulceration, dilatation 




and prolapse of the stomach, and aneurism of the abdominal 
aorta. As likely causes of pain in either hypochondrium pleurisy, 
pneumonia, subphrenic abscess, peritonitis, gastric cancer, renal 



EXAMINATION OF THE THORAX 



121 



colic, and nephroptosis are to be recalled. Pain localized along 
the upper part of the costal arch may be symptomatic of dia- 
phragmatic pleurisy, or it may come from the strain of long- 
continued coughing or retching. 

Pain in the lateral wall of the thorax is "particularly significant of 
pleurisy, pleurodynia, and intercostal neuralgia, and in this region 
may also be felt the pain of pericarditis, thoracic aneurism, mediastinal 
disease, and lesions of the vertebrae. Herpes zoster accounts for 
exquisite pain in the lateral thorax, especially on the right side. The 



Arterial hypertension ; 
constipation ; gastric 
lesions. 



Gastric ulcer 



Splenitis: pancreatit 



Sm - 




Pericarditis ; phrenic 

pleurisy. 



Hepatic disease. 



Thoracic aneurism ; me- 
diastinal disease ; gas- 
trointestinal, esopha- 
geal, and pancreatic 
lesions. 

Colonic lesions. 

Renal disease. 



leurisy; appendicitis; 
abdominal neoplasm ; 
| lumbago. 

Pelvic disease ; sacro- 
iliac and hip-joint dis- 
ease; rectal lesions. 



Fig. 68. — Areas of dorsal tenderness and pain. 



discomfort attending gaseous distention of the stomach and colon, 
as well as that of fecal impaction of the colon, is also referred to the 
side of the chest in many instances. Indefinite pains in the side are 
a common complaint in hysteric and in anemic states. 

Pain in the posterior thoracic wall (Fig. 68), if localized between the 
scapulae at the level of their spines, may mean either pericarditis or 
diaphragmatic pleurisy; at the inferior angle of the left scapula, spleni- 
tis; and at the inferior angle of the right scapula, disease of the liver. 



122 



PHYSICAL DIAGNOSIS 



In phthisis an interlobar pleurisy commonly provokes a dull ache, 
changed by coughing to a sharp, lancinating pain alongside the spine, 
at the level of the second or third thoracic vertebra, or the point cor- 
responding to the inner border of the oblique fissure between the 
upper and lower pulmonary lobes. Pain between the scapulae is 
frequently due to some disorder of the stomach, such as overdisten- 
tion, inflammation, or ulceration; tenderness at the left of the spine 
at the level of the eleventh and twelfth thoracic vertebrae is frequently 
elicited in gastric ulcer. The gnawing pain of an aneurism of the 
descending aorta is felt between the left scapula and the spinal 
column. 

Here also may be mentioned the principal factors of pain in the 
loin and in the sacral region. Aching and pain in the lumbar region, 
usually radiating to the flanks, constitute a familiar symptom in 
lumbago, lumbar neuralgia, dysmenorrhea, lithemia, and in con- 




Fig. 69.— Empyema necessitatis (Jefferson Hospital). 

ditions of simple exhaustion and neurasthenia; it may be a sign of a 
more grave disorder— renal lesions, lumbar abscess, appendicitis, 
hernia, and abdominal aneurism or neoplasm; or it may be referred 
to diseases of the bladder, the prostate, the perineum, and the rectum. 
The lumbar region is the favorite seat of the dragging ache excited 
by a mass of feces within the colon, and of the pain which attends 
many of the acute febrile infections. 



EXAMINATION OF THE THORAX 1 23 

Pain in the region of the sacrum is a finding which points perti- 
nently to diseases of the pelvis and its viscera , and one which also 
suggests sciatica, sacral neuralgia, sacro-iliac disease, coxalgia, in- 
flammation, ulcer, cancer of the rectum, and diseases of the testes. 
Of the foregoing, sciataca and lesions of the pelvis and the rectum 
also reflect pain to the outer and posterior aspects of the thigh. In 
the coccygeal region pain is attributable to such factors as coccygo- 
dynia, hemorrhoids, proctitis, and fissure or fistula of the rectum. 

Scars. — Scarring of the chest- wall and of the neck is to be carefully 
investigated, for such marks are sometimes a valuable clue in identify- 
ing questionable cases of syphilis and of tuberculosis. The cicatrix 
left by a healed perforative empyema, by a rib resection, by a trauma, 
or by a burn may also throw light upon the patient's condition. The 
pitting of variola and of varicella, the tough, thick, flat scars of lupus, 
and the minute depressions of acne are also rather distinctive. 

Other signs, noted on inspection of the cutaneous surface in general, 
rather than that of the thorax in particular, relate to the temperature 
and moisture of the skin, to deviations from its normal color, such 
as pallor, flushing, undue redness, jaundice, and pigmentation, and 
to the presence of petechiae, ecchymoses, and various eruptions. 

Clubbed or Drumstick Fingers. — Extreme incurving of the nails, 
thickening of the joints, and bulbous enlargement of the tips of the 
terminal phalanges are the hall-marks of this deformity, observed 
in various chronic diseases of the heart and the bronchopulmonary 
system, and in conditions of habitual cyanosis. Phthisis, bron- 
chiectasis, empyema, chronic adhesive pleurisy, pulmonary stenosis, 
and cardiac septal defects are prominent factors of drumstick fin- 
gers, which, with less frequency, also occur in rickets, hepatic cirrho- 
sis, gastrectasis, and myxedema. Clubbing of the fingers, with 
bilateral enlargement of the hands, feet, and long bones, is distinctive 
of Marie's hypertrophic pulmonary osteo-arthropathy, a form of 
toxic osteoperiostitis incident to various purulent lesions of the 
bronchi, lungs, and pleura. 



SECTION III 

EXAMINATION OF THE BRONCHOPULMONARY 

SYSTEM 



CLINICAL ANATOMY 

The Lungs.— The lungs are a pair of roughly pyramidal organs, 
closely approximated to the walls of the pleural cavity, their bluntly 
convex apices occupying the pleural domes, and their broad, concave 




Fig. 70. — Radiograph of the normal thorax. (Plate by Dr 



Manges.) 






IS 



bases resting upon the diaphragm. Of the two lungs, the left 
somewhat longer, narrower, and less voluminous than the right. 

The outer or costal surf aces of the lungs, which are convex, are closely 
adapted to the inner pleural surfaces of the ribs and the intercostal 
spaces. The inner or mediastinal surfaces bound the mediastinum 
124 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 25 

and are deeply indented, especially on the left side, to afford room 
for the heart. Above and behind this hollow space is the wedge- 
shaped hilus of the lung, within which the bronchi, the pulmonary 
artery, pulmonary veins and nerves, the bronchial vessels, and the 
lymphatics communicate with the lungs. These structures, entering 
and leaving at the hilus, constitute the root of the lung, which lies 
opposite the fourth, fifth, and sixth thoracic vertebrae. The inner 
pulmonary surfaces are grooved on the right side for the superior vena 




Fig. 7 1 - — Anterior surface topography of the lungs, bronchi, and pleura;. 



cava, the vena azygos major, and the innominate vessels; and on the 
left side for the aorta, the subclavian artery, and the innominate 
vein. Anchored only by its root and ligamentum latum pulmonis, 
each lung is otherwise unattached to its pleural space, in which, 
therefore, it has unhampered motility. 

The apices of the lungs rise from J to ij inches (1.25 to 3.75 cm.) 
above the clavicles, the right apex being about \ inch (1.25 cm.) higher 
than the left. From the apex the anterior border of the right lung 
is traced by a line running through the sternoclavicular articulation 



126 



PHYSICAL DIAGNOSIS 



to the midsternal line, at the level of the. second chondrosternal joint, 
from which point it drops vertically downward to the level of the sixth 
costal cartilage. The anterior border of the left lung corresponds to 
that of the right as far down as the fourth costal cartilage, but at this 
level it curves outward along the lower border of the fourth rib as 
far as the parasternal line, then drops vertically downward to the 
upper border of the.fifth rib, and courses inward to a point upon the 




Fig. 72.— Posterior surface topography of lungs, bronchi, and pleurae. 

upper border of the sixth costal cartilage, just inside the parasternal 
line. This notched contour of the left anterior pulmonary margin 
overlies the right ventricle, which, uncovered by lung tissue, corre- 
sponds to the area of superficial cardiac dulness, or cardiac flatness. 

The lower borders of the lungs are represented by a line running 
outward from each lower extremity of the anterior border, and, coin- 
ciding with the sixth rib in the midclavicular line, the eighth rib in 
the midaxillary line, the tenth rib in the scapular line, and the tenth 
thoracic vertebra in the midspinal line. Since the inferior margin of 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 27 



the right and the left lung may be considered identical clinically, the 
foregoing surface-marking applies to each. 

The three lobes of the right lung are indicated by the courses of 
its oblique and horizontal fissures, while the two lobes of the left 
lung are separated by its single fissure, the oblique. The position 
of the oblique fissures, which is the same in each lung, is marked by 






Fig. 73 — Right lateral surface topog- 
raphy of the lungs and pleurae. 



Fig. 74.— Left lateral surface topog- 
raphy of the lungs and pleurae. 



a line beginning at the second thoracic spinous process, continuing 
downward and forward through the root of the scapular spine to the 
fourth rib in the midaxillary line, and terminating at the lower border 
of the lung at the sixth costal cartilage, just inside the parasternal line. 
The line of the horizontal fissure of the right lung begins at the anterior 
pulmonary border at the level of the fourth costal cartilage, and 
extends outward below the fourth rib as far as the midaxillary line, 
where it joins the oblique fissure. 

Making use of these interlobar landmarks, the following limits of 
the pulmonary lobes can be mapped out upon the surface of the 



128 PHYSICAL DIAGNOSIS 

body: The right anterior thorax overlies the upper lobe from the 
supraclavicular space to the fourth rib; the middle lobe, from the 
fourth to the sixth ribs; and a triangular portion of the lower lobe, 
below and outside the latter level. Upon the left anterior thorax 
the upper lobe extends downward as far as the junction of the sixth 
costal cartilage and the lower pulmonary border, below which level 
the lower lobe extends to the left. Upon the right lateral thorax 
the point at which the midaxillary line crosses the fourth rib marks 
the junction of the upper, the middle, and the lower lobes. The 
same point upon the left lateral thorax divides the upper and the 
lower lobes of the left lung. Upon the posterior thorax on each side 
the greater part of the upper lobe lies above the scapular spine, below 
which i* the lower lobe, extending downward to the level of the tenth 
thoracic vertebra. 

The Bronchi and Trachea. — The trachea begins at the lower 
border of the cricoid cartilage, enters the mediastinal space at the 
level of the seventh cervical vertebra, and terminates by division into 
the right, and left primary bronchial tubes, at the level of the root 
of the scapular spine posteriorly, or at the angle of Louis anteriorly. 
The bronchi extend obliquely downward and outward from the 
bifurcation of the trachea to the root of each lung, the right bronchus 
entering the corresponding lung at a somewhat higher level than the 
left. The right bronchus differs from the left in being shorter, of 
larger diameter, and of more vertical course — hence the relatively 
exaggerated physical signs over this tube, as well as its greater pre- 
dilection for foreign bodies that pass below the division of the wind- 
pipe. The bronchial lymphatic glands, which are especially numer- 
ous near the tracheobronchial junction, extend along each bronchial 
tube toward the root of the lung. These glands, when tuberculous 
or otherwise diseased, may, by pressure, inflammation, and infec- 
tion, seriously implicate the bronchi, the trachea, the esophagus, 
and the pericardium. 

The Pleurae. — The pleural cavities, which contain the lungs, are 
lined each with a separate pleural membrane, one layer being in 
intimate relation with the thoracic parietes (parietal pleura), and a 
second layer closely investing the lungs (visceral pleura). The 
parietal pleura, though a continuous membrane, is arbitrarily divided 
into several parts (cervical, costal, diaphragmatic, mediastinal), 
corresponding to different areas of the thoracic chamber. The sig- 
nificance of these artificial divisions of the pleural covering is self- 
evident. The visceral pleura closely adheres to the lung, both upon 
its external and interlobar surfaces, and at the pulmonary root it 
becomes continuous with the mediastinal part of the parietal pleura. 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 29 

The surface line of the right pleura extends anteriorly from the 
sternoclavicular articulation to the level of the second chondrosternal 
joint at the left of the midsternal line, whence it continues downward 
to the ensiform process, and then is deflected to the right, crossing 
the lower border of the seventh rib in the midclavicular line, the tenth 
rib in the midaxillary line, and the upper border of the twelfth thoracic 
vertebra at the spine. The line of the left pleura descends from the 
left sternoclavicular joint parallel to the course of the right pleura, 
running beneath the outer third of the sternum as far as the fourth 
rib; at this level, however, it turns obliquely to the left sternal edge, 
beneath which it resumes a vertically downward course to a point 
in the middle of the sixth costal cartilage; thence the line follows, 
at a somewhat lower level, the same course as the pleural line of the 
right side to the vertebral column. Posteriorly, both pleurae parallel 
the spine from the first to the twelfth thoracic vertebra. 

The space lying between the two pleurae beneath the sternum 
corresponds to the situation of the anterior mediastinum. The 
apex of the pleural cavity, inclosing the pulmonary apex, is bounded 
by a pyramidal line running from the sternoclavicular joint to meet 
the posterior pleural border at the level of the first thoracic vertebra 
posteriorly. The slight outward deviation of the left anterior pleural 
line below the fourth rib exposes the pericardium to immediate con- 
tact with the sternum. The recess intervening between the lower 
pulmonary and pleural borders is known as the complementary 
pleural space; this sinus, largely occupied by the lungs when they are 
fully inflated, during their deflation varies in depth from ij to 3^ 
inches (3.75 to 8.75 cm.), being deepest on the lateral chest- wall, and 
extends vertically from about the sixth to the seventh rib in the 
midclavicular line, from the eighth or ninth to the tenth rib in the 
midaxillary line, and from the tenth to the twelfth thoracic vertebra 
in the midspinal line. 

The Mediastinum. — The intrapleural space, extending from the 
sternum to the spine, and partitioning the cavity of the chest 
into two lateral compartments inclosing the lungs and pleurae, is 
termed the mediastinum thoracis, or the mediastinal space. The 
pleural surfaces surrounding this space are continuous with the costal 
pleurae above the superior outlet of the thorax, while at its base the 
mediastinum is attached to the diaphragm. The important structures 
inclosed by the mediastinum include the heart and its great vascular 
trunks, the trachea, esophagus, and thoracic duct, the thymus gland 
or its remnants, the bronchial and mediastinal glands, and the 
pneumogastric and phrenic nerves. It is convenient, for the sake 
of clear description, to divide the mediastinum into four arbitrary 



130 



PHYSICAL DIAGNOSIS 



spaces,— superior, middle, anterior, and posterior, — upon whose 
anatomic differences the interpretation of mediastinal physical signs 
is to be based. 

The superior mediastinum lies above the pericardium, and is 
bounded anteriorly by the manubrium sterni, posteriorly by the 
bodies of the first four thoracic vertebrae, inferiorly by a line drawn 
obliquely from the lower border of the fourth thoracic vertebra to that 
of the manubrium, and laterally by the mediastinal pleurae. This 
section of the mediastinum contains the aortic arch, and the innomi- 
nate, left common carotid, and left subclavian arteries; the upper 
part of the superior vena cava and the innominate veins; the trachea, 
esophagus, and thoracic duct; the remains of the thymus gland and 
the superior mediastinal glands; and the phrenic, pneumogastric, 
left recurrent laryngeal, and cardiac nerves. 

The middle mediastinum comprises the enlarged central portion 
corresponding to the pericardium and heart, in addition to which this 
space also contains the ascending aorta and its branches, the pul- 
monary artery, the lower part of the superior vena cava and the vena 
azygos major, the bronchial lymphatic glands, and the phrenic nerves 
with their accompanying vessels. 

The anterior mediastinum is a triangularly shaped space between 
the sternum and the pericardium, extending vertically from the lower 
border of the manubrium to the sixth or . seventh costal cartilages. 
It incloses merely a group of lymphatic glands, the anterior medias- 
tinal, embedded in areolar tissue. 

The posterior mediastinum, which is virtually a downward exten- 
sion of the superior space, lies between the posterior surface of the 
pericardium and the spine, and corresponds to the bodies of the eight 
lower thoracic vertebrae. The contents of this space are the de- 
scending thoracic aorta, the azygos veins, the esophagus, the 
thoracic duct, the pneumogastric nerves, and the posterior medias- 
tinal lymphatic glands. 

INSPECTION 

Inspection bears importantly upon the diagnosis of pulmonary 
diseases, the evidences of which are in some instances clearly shown 
by anomalies in the configuration of the chest and in the character 
of its respiratory movements. Cyanosis, edema, lymphadenitis, 
and enlargement of the superficial veins are additional signs, often- 
times secondary to lesions of the lungs. These physical signs have 
been dealt with in the preceding section (p. 106 et seq.), and, there- 
fore, require no further mention here. 

The examiner should investigate the thorax systematically from 






EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 13I 

every point of view — from the front, from the sides, from behind, 
and from above downward, standing behind the patient and looking 
down over the clavicles. The patient, preferably stripped to the 
waist, is placed in such a position that the light falls directly upon 
the surface to be examined, save when some inconspicuous sign, such 
as a small patch of deficient expansion or an ill-defined pulsation, 
is sought for, in which event oblique illumination is better. The 
importance of routine inspection of the chest cannot be insisted upon 
too emphatically in every case in which there is reason to suspect a 
pulmonary disorder. 

The respiratory turgescence of the cervical veins is sometimes 
an aid in the diagnosis of infiltrations and new-growths of the anterior 
mediastinum. Normally, forcible expiration with the mouth and 
the nares closed (Valsalva's method) dilates these vessels equally 
on either side, but should the intrathoracic venous trunks be com- 
pressed, the cervical veins on the affected side dilate sooner and 
more conspicuously than those on the opposite side of the neck. 

The pressure of a mass of enlarged bronchial glands may cause 
venous suffusion of the neck when the patient's head is forced far 
backward in the median line, thereby exerting upon the air-tubes 
sufficient traction to force the glandular tumor against the cervical 
vessels. 

Circumscribed areas of pulsation, aside from those of precordial 
origin, elsewhere described (p. 329), are met with in certain diseases 
of the lungs and pleura. Pulsating pleurisy, usually of the purulent 
type, may account for a throbbing or an undulation in one or more 
interspaces, almost invariably on the left side, between the second 
and the sixth ribs. An intrathoracic pulsating neoplasm, by encroach- 
ing upon the inner chest-wall, may also produce a rhythmic surface 
throb. A large cavity of the left lung, which abuts directly against 
the heart, may, by conduction of the cardiac impulse, account for a 
systolic throbbing over the lower lobe posteriorly (Steven). 

Displacement of the larynx, recognized by deviation of the 
pomum Adami from its median position, occurs in consequence of 
intrathoracic lesions that either drag or push the trachea from its 
normal course. Extensive pleural effusion, pneumothorax, thoracic 
aneurism, mediastinal neoplasm, pulmonary excavation and even 
a circumscribed dilatation of the aortic arch are to be thought of 
as possible factors of this deformity. Displacement of the larynx 
by an adjacent growth {i. e., a thyroid tumor) is readily distin- 
guished from that due to the conditions just noted. 

Inequality in the size of the pupils is a pertinent sign in certain 
diseases of the lungs and pleura, as in unilateral phthisis, pleurisy, 



I 3 2 



PHYSICAL DIAGNOSIS 



and other lesions exciting irritation of the sympathetic nerve, 
as shown by a relatively wider pupil on the affected side. Grober 
emphasizes the significance of deviations from the normal expiratory 
contraction and inspiratory dilatation of the pupils. With Valsalva's 
method of breathing the dilatation of one pupil with expiration 
(bilateral contraction being normal) suggests a circumscribed lesion 
on the same side; while if both pupils dilate (instead of contracting), 
bilateral disease is to be inferred — inferred, but not assumed, for 
the value of these pupillary signs is to be decided only in the light of 
a full clinical inquiry. The absence of such changes by no means 
warrants the exclusion of thoracic disease. 

PALPATION 

In examining the lungs the sense of touch is used chiefly to 
study various sorts of fremitus, or vibrations felt over the pulmonary 




Fig- 75- — Technic of palpating the pulmonary apices. 

structure, the pleurae, and the bronchi when the subject speaks, 
breathes, or coughs, as the case may be. In addition, palpation not 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 133 

only confirms the signs afforded by inspection, but in many instances 
it proves even more definite, as, for example, in recognizing defi- 
ciencies of expansion and local asymmetry so slight as to be overlooked 
by the eye. Different chest pains and areas of circumscribed tender- 
ness — pleural, neuralgic, muscular — are traced to their proper 
sources by palpation with much greater surety than when the patient's 
statement alone is relied upon. Tracheal tugging, to be described 
subsequently, is occasionally detected when adhesions exist between 
the trachea or the large bronchi and a neoplasm of the mediastinum, 
though more commonly this sign is 
symptomatic of aneurism of the aor- 
tic arch (q. v.). 

In performing palpation the hands 
should be applied, palms downward, 
to the naked skin, and moved from 
place to place methodically, so as to 
cover the entire surface of the thorax, 
care being taken to compare the dif- 
ferences of the two sides, especially 
at the apices and at the bases. Aim- 
less, wandering palpation is worse 
than none at all, and unless the ex- 
amination be systematic and com- 
parative, the results will be mislead- 
ing and confusing. Lagging respir- 
atory movements at the apex are 
readily appreciated if the examiner 
stands behind the patient with his 
index- and middle fingers applied to 

the supraclavicular and infraclavic- ™ „ , , ,, , 

, . . ,„ v Fig. 75a. — Betneas method 

ular spaces, respectively (Fig. 75), of determining apical expan- 

or, observing the same posture, the sion. 
examiner, with hands applied to the 

subject's axillae, determines with the finger-tips the relative ex- 
tent of the respiratory (excursion) at the level of the second or 
third ribs, Bethea's method (Fig. 75a). Deficient expansion at 
the bases is well determined by facing the patient with the hands 
closely pressed against the curve of the lower dorsolateral regions 
of the chest. In gaging the relative expansibility of the lower 
parts of the thorax F. A. Craig advises the examiner to stand 
behind the subject, firmly grasping the axillary regions, with the 




134 



PHYSICAL DIAGNOSIS 



thumbs pointing toward the spine, noting the distance during 
forced inspiration from the spinous processes to the right and the 
left thumbs. 

To gage the general chest expansion, the examiner should stand 
at the subject's side, placing one hand upon the sternum and the 
other between the scapulae. 

Vocal Fremitus. — Vocal fremitus is the tactile vibration appre- 
ciated by the hand applied to the chest-wall while the patient is 
speaking aloud. The vibrations thus felt arise in the vocal cords, 
whence they travel via the trachea, the bronchi, the vesicular structure, 
and the parietes to the surface of the thorax, where they are recog- 
nized as a peculiar purring vibratory sensation. 

In eliciting vocal fremitus the palm of the hand is pressed firmly 
against the bared chest of the patient, who is instructed to repeat, 
in a deep voice, " ninety-nine," or to count "one, two, three" a number 
of times, the resulting vibrations being appreciated by the palmar 
surfaces of the examiner's fingers. Or, as Berkeley suggests, the 
sound of "66," as in "moon" or "rood," is excellent for tactile 
purposes. Ulnar palpation, or the application of the ulnar side of 
the hand, is recommended by some clinicians, but it seems far infe- 
rior to the palmar method, owing to the much less delicate tactile 
sensibility of the side of the hand as compared to that of the fin- 
cers. Comparative tests of the fremitus of both halves of the 
chest should always be practised, in order to detect slight differ- 
ences. The intensity of the vibrations depends upon the loud- 
ness and the pitch of the voice, and upon the conducting qualities 
of the structures between the larynx and the palpator's hand. It 
is more intense in adults than in children; in men than in women; 
in persons of loud, low-pitched, harsh voice than in those whose 
voice is quiet, high-pitched, and soft; and in the thin, spare indi- 
vidual than in one whose chest is muscular, fat, or edematous. 
The comparative intensity of vocal fremitus over different regions 
of the chest is shown by Figs. 76 and 77. 

Normally, vocal fremitus is relatively exaggerated over the right 
side of the thorax, especially in the infraclavicular and interscapular 
regions. This disparity between the fremitus of the two sides is 
explained partly by the larger caliber and the less acute bronchotrach- 
eal angle of the right bronchus, and partly by the fact that the tube 
leading to the right upper lobe arises closer to the trachea and at a 
higher point than the corresponding left tube — anatomic differences 
by virtue of which the volume of vibrations is greater, their route 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 135 

shorter, and their transmission less impeded within the bronchus of 
the right lung than within that of the left. The intimate anatomic 
relation of the trachea and the right lung is another factor of right- 
sided exaggeration of the fremitus, as recently shown by Fetterolf . 
Lateral decubitus also influences the intensity of the voice vibra- 
tions, the side of the chest in contact with the bed affording a 
perceptible increase of both vocal fremitus and resonance, together 




Fig. 76. — Comparative intensity of vocal fremitus, vocal resonance, and respir- 
atory sounds over the anterior thorax. 



with a commensurate modification of pulmonary percussion reso- 
nance and a slight exaggeration of the respiratory murmur. 

The vocal fremitus is faint over the scapulae, the sternum, and 
the female mammae, owing to the interference of these parts with the 
conduction of the vibratory waves. These latter are, of course, 
absent over the areas of the thorax corresponding to the immediate 
contact of the heart, liver, and the spleen. On the other hand, 
the voice vibrations are clearly conducted by the clavicle, and can 
be distinctly palpated as far as its outer extremity. 



136 



PHYSICAL DIAGNOSIS 



Increased Vocal Fremitus .—This is found in croupous pneumonia, 
diffuse catarrhal pneumonia, tuberculous infiltration, infarction, 

and fibrosis, since consolida- 

"1 tions such as these conduct 
vibrations with undue power; 
the same thing occurs in the 
case of a dense intrathor- 
acic neoplasm situated near a 
bronchus. An interpleural 
fibrous band will telephone 
voice fremitus through a 
pleural effusion, notwithstand- 
ing the non-conducting prop- 
erties of the latter (v. i.) . In- 
creased pulmonary tension, 
which favors clear transmis- 
sion of the sound-waves, ex- 
plains the exaggerated frem- 
itus incident to congestion of 
the lungs. A cavity, either 
pulmonary or bronchial, am- 
plifies the voice vibrations 
and, therefore, increases the 
fremitus, but to act thus as 

J 1 resonating chamber the 
„ . . cavity must be near the surface 

Fig. 77. — Comparative intensity of vocal J 

fremitus, vocal resonance, and respiratory and of considerable Size, With 

sounds over the posterior thorax. resilient walls and a patent 

bronchial communication. 
Decreased Vocal Fremitus. — Modifications of vocal fremitus, 
ranging from slight enfeeblement to actual abolition of the vibrations, 
occur as the result of subnormal pulmonary tension, pleural effusions 
and thickening, and bronchial obstruction. Hypertrophic emphy- 
sema, which diminishes the tension and the resiliency of the lungs, 
weakens the transmission of the voice vibrations, but scarcely to the 
extent popularly supposed, and, by a similar mechanism, pulmonary 
edema has the same effect on fremitus. A plural cavity containing 
either air or liquid interferes with vocal fremitus, in consequence of 
the non-conducting properties of the effusion and because of the 
associated pulmonary relaxation. A greatly thickened pleura or 
one bathed in a thick, buttery exudate also weakens the vocal vibra- 
tions. If any part of the bronchial tubes be blocked, the vocal fre- 




EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 137 

mitus over the pulmonary area communicating with the occluded 
part of the bronchial tree is correspondingly diminished. This occurs 
as the result of spasm of the tubes, inflammatory swelling of their 
mucosa, and mechanical obstruction of their lumen by a foreign 
body or by the pressure of an aneurism, a neoplasm, or a glandular 
mass. Or the occlusion may be spastic or exudative, as in diffuse 
catarrhal bronchitis, fibrinous bronchitis, and asthma. It is import- 
ant to note that in croupous pneumonia, despite the consolidation, 
vocal fremitus may be completely abolished over the pneumonic 
lobe if the bronchus leading thereto happens to be plugged with a 
mass of fibrin. 

Rhonchal Fremitus. — The vibrations of coarse bronchial and 
tracheal rales are sometimes felt upon the surface of the chest, especi- 
ally during inspiration. This rhonchal or bronchial fremitus is to be 
looked for in bronchitis and in asthma, and is particularly common 
in the bronchitis of young children. It is, of course, abolished by 
bronchial occlusion, and is influenced by coughing and by deep 
respiration. Occasionally tactile fremitus due to cavernous rales 
is appreciable over pulmonary and bronchial cavities. 

Succussion Fremitus.— This sign, the tactile equivalent of the 
Hippocratic succussion sound, may occur over a pleural cavity con- 
taining air and fluid when the subject's chest receives a sudden jar, 
so as to splash a wave of fluid against the inner chest-wall. 

Tussile Fremitus. — The palpable vibrations excited by coughing 
are known as tussile or tussive fremitus. They are of trifling clinical 
value, save perhaps in cases of aphonia, in which it is impossible to 
elicit vocal fremitus. 

Friction Fremitus. — Tactile vibrations corresponding to the 
pleural friction-sound are sometimes detected over roughened pleural 
surfaces when the patient takes a deep breath. This pleural friction 
fremitus feels superficial to the palpating hand, is affected by firm 
pressure and by forcible respiration, and has a fine, rasping, or even 
creaking quality, according to the character of underlying pleural 
lesion. (Cf. Pericardial Friction, p. 397.) 

Increased Resistance and Fluctuation. — The increased surface 
resistance over pleural thickening, pleural effusions, and pulmonary 
consolidations is appreciable by palpation as well as by percussion. 
Less commonly the resistance is increased by the diminished elasticity 
of the lungs incident to extreme emphysema and to pneumothorax. 
Increased rigidity of the thoracic parietes causes a corresponding 
increase in the degree of resistance upon the surface. 

In exceptional cases pitting and even circumscribed fluctuation 



138 PHYSICAL DIAGNOSIS 

due to an affection of the lungs or pleura can be felt upon the surface 
of the thorax, as in the preperforative stage of empyema necessitatis, 
and in pulmonary hydatid cyst, inflamed and about to fistulate through 
the chest-wall. Under the latter circumstance hydatid fremitus 
is sometimes demonstrable by laying the fingers, widely separated, 
over the swelling, and sharply percussing upon one of them, where- 
upon a delicate thrill, due to the impact of the daughter cysts, is 
appreciated by the other three ringers. This so-called hydatid 
fremitus or thrill must be distinguished from muscular fremitus 
(Barnabei) arising from fibrillary muscular contractions set up by 
manual stimulation. Such fremitus is especially prone to occur in 
the abdominal muscles in connection with conditions of excessive 
intraperitoneal tension, and, unlike true hydatid fremitus, can be 
excited at will, merely by deep, kneading palpation. 

PERCUSSION 

Percussion of the lungs gives information relating to the extent 
of the pulmonary or vesicular resonance and its pathologic modifica- 
tions, due to lesions of the lungs and their pleural investment, such 
lesions including consolidation, collapse, overdistention, and excava- 
tion of the vesicular structure, together with pleural thickening and 
collections, gaseous or fluid, within the pleural sacs. 

The general rules regarding the patient's symmetric posture, 
muscular relaxation, and quiet respiration (see p. 27) are to 
be observed, in order successfully to practise pulmonary percus- 
sion. In examining a bed-ridden person perfect anatomic sym- 
metry of the parts is a preliminary essential to the best results, whether 
the subject be in the dorsal, the ventral, or the lateral decubitus. 
In percussing the anterior chest-wall of a patient in the upright 
position his head should be kept in the median line, with the arms 
hanging naturally at the side, so as to poise the trunk symmetrically 
(Fig. 1) . In percussing the back the subject should bend well forward 
from the waist, and fold the arms across the chest, in order to tilt 
forward the scapulae, thus flattening the posterior thoracic wall and 
exposing as large an area of it as possible; or the patient may lean 
forward in the position illustrated below (Fig. 78). The lateral 
regions of the thorax are made accessible by having the subject raise 
the arms, with the clasped hands resting upon the top of the head. 
Percussion of the apices is not an easy matter, owing chiefly to the 
dulling effect of the thick musculature of the neck, and to the adja- 
cent tympanicity of the trachea. The apices may be percussed from 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 39 

before, with the little finger applied as a pleximeter to the supra- 
clavicular space above and parallel to the clavicle (Fig. 79), or from 
behind, with the pleximeter finger pointing toward the sternoclavic- 
ular joint (Fig. 80). 

In comparative percussion the areas to be contrasted should be 
percussed during the same respiratory stage, the force of the blow, 




Fig. 78. — Technic of percussing the posterior thorax. 

the pressure of the pleximeter finger, and the other details of the 
percussion technic being identical. Furthermore, the comparable 
parts must be of similar anatomic structure — the sound obtained 
over an interspace should be compared with that elicited over a 
corresponding interspace, not with the sound over a rib or over a 
dense muscle. 

By respiratory percussion certain respiratory differences in the per- 
cussion sounds can be judged by percussing over the same area while 
the subject holds the breath, first, after deeply inflating, and then 
after similarly deflating, the lungs. Normally, when the breath is 
held after a full inspiration, the sound is of greater resonance, more 
volume, and higher pitch than that elicited after a forced expiration, 
these differences being particularly clear on the right side, below the 
clavicle and above the scapula. 

Normal Pulmonary or Vesicular Resonance. — The distinctive 
hall-mark of pulmonary resonance is its quality, which, being sui 
generis, is comparable only to the sound excited by the vibration of 



IAO 



PHYSICAL DIAGNOSIS 



healthy pulmonary tissue having an air-content distributed through 
innumerable minutely divided alveolar spaces. Experience alone 




Fig. 79-— Technic of percussing the pulmonary apices. 



will enable one to recognize this characteristic vesicular quality, which 
dominates the pulmonary percussion sound, irrespective of its pitch, 
intensity, and duration. These acoustic details of resonance have 
been considered in a preceding section. (See p. 17.) 

Certain regional differences in normal pulmonary resonance, due 
entirely to physiologic causes, must be clearly distinguished, in order 
not to misinterpret the results of percussion of the lungs. Modifica- 
tions of the percussion sound, perfectly normal in one region of the 
chest, may be pathologic when found in a different area, so that the 
significance of any given sound rests upon its variance from the sound 
afforded by the part in health. 

The clear, low pitch and vesicular quality of pulmonary resonance 
are typically illustrated by percussing in the upper axillary region 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 141 

above the fourth rib, and this is also true of the middle of the 
infraclavicular region; at the sternal end of this region, however, 
the resonance ot the lung blends with the osteal tone of the 
sternum and with the tympanitic element of the underlying pri- 
mary bronchi and trachea. Owing to the anatomic peculiarities 
of the right bronchus and to the encroachment of the large 
blood-vessels upon the right pulmonary apex (Norris; Fetterolf), 
the percussion sound is somewhat higher pitched and less typ- 
ically vesicular in the right than in the left infraclavicular area. 




Fig. 80. — Technic of percussing the pulmonary apices. 



To a minor degree these differences are also found in the supra- 
clavicular regions, at the inner portions of which one must reckon 
with tracheal tympany. 

Anteriorly, on the right side, the dulling effect of the liver is encoun- 
tered in the midclavicular line below the fourth rib, and in the anterior 
axillary line below the sixth rib. On the left side, below the fourth 
rib, the dulness of the heart modifies the pulmonary sound within the 
midclavicular line, while between this line and the axilla the influence 
of gastric tympany is apparent below the fifth rib. On both sides 



142 PHYSICAL DIAGNOSIS 

resonance is obscured over the site of the great pectoral muscles 
and the mammary glands. Laterally, hepatic dulness on the right 
side, and gastric tympany (perhaps, also, splenic dulness) on the left 
side, modify the resonance of the lower axillae. Posteriorly, the 
percussion sound is nowhere so resonant as it is anteriorly, this being 
especially noticeable -above and over the scapulae, where the dead- 
ening effect of the bone is obvious. In the other regions of the back 
resonance is more or less obscured by the thick musculature, the 
spine, and the underlying solid viscera. 

Aside from the foregoing differences, it must be remembered that 
pulmonary resonance is obscured wherever the thorax bears a dense 
investment of muscle or of fat, and also that undue rigidity of the 
bony thorax lends impurity to the percussion sound. Postural 
compression of one side of the thorax may cause dulness due to 
mechanical suppression of parietal vibrations. (See p. 135.) 

Normal Limits of the Pulmonary Borders (Figs. 71, 72, 73, 
and 74) . — The position of the pulmonary borders is determined by 
percussion while the subject's lungs are in a state of median inflation, 
i. e., during respiratory repose. The upper borders are outlined by 
percussion over the supraclavicular spaces, where the apices project, 
in health, from \ to 1^ inches (1.25 to 3.75 cm.) above the clavicles. 
The lower borders are mapped out by percussing vertically downward 
along the midclavicular, the midaxillary, and the scapular lines, from 
typical pulmonary resonance to the levels of hepatic flatness on the 
right side, and to gastric tympany and the flatness of the spleen, the 
kidney, and the lumbar muscles on the left side. The lower border 
of the right lung extends to the sixth rib in the midclavicular line, to 
the eighth rib in the midaxillary line, and to the tenth rib in the scapu- 
lar line, hepatic flatness lying below these levels. The lower border 
of the left lung extends in the midclavicular line to the sixth rib or 
interspace, below which there is the sound of gastric tympany, while 
the lateral and the posterior levels of the left lower border are prac- 
tically the same as those of the right lung. The anterior borders of 
the lungs are too closely approximated to be separated by percussion, 
and the excessive vibrations of the sternum, beneath which these 
borders lie, also forbid their delimitation. The peculiar curve of 
the precordial border of the left lung bounds the area of cardiac 
flatness lying at the left sternal margin, between the fourth and sixth 
ribs. (See Cardiac Percussion, p. 358.) 

In early childhood the lower pulmonary borders are higher, and 
in advanced life lower, than the above mean levels, the difference in 






EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 43 

each instance amounting to about 1 inch (2.5 cm.) . Changing from 
the dorsal to the lateral decubitus depresses the lower border of the 
uppermost lung about 1^ inches (3.75 cm.) in the axilla, and changing 
from the dorsal to the erect posture elevates the lower level \ inch 
(1.25 cm.) anteriorly. 

Changes in the Mobility and Position of the Pulmonary 
Borders. — The mobility of the lungs is gaged by the excursions of 
the pulmonary borders, as shown by their positions during extreme 
inspiration and expiration. In the healthy adult the vertical excursion 
of the lower border above and below the mean is about 1^ inches 
(3.75 cm.) anteriorly, and 3 inches (7.5 cm.) laterally, the inspiratory 
convergence of the anterior borders encroaching upon precordial 
flatness practically to the point of obliteration. Restriction, in part 
or absolute, of this excursion is noted should the lungs be overdis- 
tended, infiltrated, or hampered by adhesions or by mechanical 
pressure. Thus, emphysema, consolidations, fibrosis, adhesive 
pleurisy, and excessive intra-abdominal pressure, by limiting the 
normal pulmonary excursions, are attended by unnaturally small 
differences between the inspiratory and the expiratory levels of the 
pulmonary borders, and in such instances the axillary diaphragm 
shadow is correspondingly obliterated. (See Litten's Sign, p. 95O 

The extent of the pulmonary resonance is determined by the 
position of the pulmonary borders during respiratory repose, devi- 
ations from the normal boundaries being either general or circum- 
scribed, according to the nature of the pulmonary lesion responsible 
for such changes. 

A general extension in the area of pulmonary resonance is met with 
in hypertrophic emphysema, in which all the normal boundaries 
of the lungs are overstepped, the apical resonance rising to 
an unnatural height above the clavicles, the basic resonance encroach- 
ing upon the upper zone of hepatic dulness, and the resonance of 
the anterior borders extending partly or completely over the cardiac 
area ordinarily uncovered by the lungs. It is in this region especially 
that an emphysematous extension of the borders is likely to be most 
readily detected. A similar extension of the pulmonary borders 
may attend an asthmatic paroxysm, fibrinous bronchitis, and dilata- 
tion of the lungs consequent to uncompensated cardiac disease. 
Circumscribed emphysema is associated with extension of the pul- 
monary resonance corresponding in situation and extent to the seat 
of the lesion. The lower pulmonary borders not uncommonly sag 
below their normal level in Glenard's disease. 



144 PHYSICAL DIAGNOSIS 

Decrease in the extent of pulmonary resonance, if general, may be 
symptomatic of atrophic emphysema; if local, some lesion provoca- 
tive of pulmonary retraction and shrinkage is suggested. Diminu- 
tion in the height of the apical resonance, unilateral or bilateral, 
points to phthisis or to pleural adhesion. A similar inference at- 
taches to the restriction of Kronig's isthmus, a narrow band of 
apical resonance extending from the clavicle to the scapular spine, 
its narrowest part being at the top of the shoulder, at which 
point it measures about 2 inches (5 cm.) in width. The outer 
boundary is represented by a line from the junction of the outer 
and middle thirds of the clavicle to the middle of the scapular spine 
and the inner limit by a line from the sternoclavicular joint to the 
level of the second thoracic vertebra. The anterior and posterior 
aspects of the area widen to approximately twice this measurement 
and blend with the pulmonary resonance of the infraclavicular and 
scapular regions. Narrowing of Kronig's isthmus is a sign of early 
apical consolidation, and as the underlying pulmonary structure 
progressively infiltrates, shrinks, and loses resilierfcy the resonant 
patch progressively diminishes and ultimately is replaced by supra- 
clavicular dulness. 

Elevation of the lower borders, with apparent extension of the 
vertical hepatic dulness, may be symptomatic of pleural retraction 
or of tuberculous or atelectatic contraction of the lung. Uni- 
lateral elevation of the lower pulmonary border is also observed in 
pneumothorax, pleurisy with effusion, paralysis of the diaphragm, 
and upward displacement of this muscle by excessive subphrenic 
pressure. Fibroid retraction affecting the anterior borders of 
the lungs may account for an unduly large area of cardiac 
dulness. 

Dulness and Flatness. — Impaired pulmonary resonance, with 
a corresponding increase in resistance, denotes airlessness, absolute 
or relative, in the structures within range of the percussion impact, 
or, as Weil expresses it, the acoustic sphere of action. This may be 
due to infiltration of the pulmonary parenchyma, to fluid within the 
pleural sac, to thickening of the pleura, or to a neoplasm situated 
directly beneath the chest-wall. Thus, dulness is found in croupous 
pneumonia, diffuse coalescing catarrhal pneumonia, phthisis, atelecta- 
sis, congestion, edema, cirrhosis, and in destructive processes of the 
lung, such as abscess, gangrene, and new-growths. The percussion 
sound is dulled to the degree of flatness as the result of pleural effusion, 
pleural thickening, enlarged bronchial glands, and neoplasms of the 
pleura and of the mediastinum (Fig. 81). 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 45 

The degree of dulness depends upon the volume of air in the parts 
percussed, upon their size and situation, and upon the force of the 
percussion stroke. Other things being equal, the larger, more super- 
ficial, and more densely consolidated the lesion, the more marked the 
degree of dulness. The influence of the above factors is well shown 
by comparing the sounds produced by strong and by light percussion 
over pulmonary infiltrations of different size, situation, and distribu- 
tion (Fig. 82). The percussion stroke may be too light to elicit 
the dulness of a deeply seated extensive consolidation, since with 
light percussion the vibrations fail to reach the airless area and, 
therefore, elicit only the resonance of the intervening normal vesicular 
structure. Strong percussion, the sphere of which includes the con- 
solidated patch, at once reveals the latter by an impairment of the 




Bronchial breathing. 
Increased vocal fremitus 
Bronchophom/jloectoriloquy- 
Tympany. 



pronehivesicuiarbrealhinq 

Increased vocal fremiti 

Increased uocal resonance 

Impaired kigk-pdcked 
1 resonance 

Bronchial breathing _ 
Increased vocal fremitus 
Increased vocal resonance 

Vul ncss. 

jJbsent breathing 
-Absent vocal fremitus - 
Jlbsent vocat resonanee 
Tldthcss 



Fig. 81. — Physical signs in pulmonary consolidation and in pleural effusion. 



resonance. Percussion may be too strong to bring out the dulness 
of a small superficial infiltration, should the blow be of sufficient force 
to set up vibrations in the lung tissue behind and around the patch, 
the dulness of which is thus obscured by the predominant resonance 
of the vesicular sound. Under the same circumstance, if the per- 
cussion stroke be light, so as to affect only the infiltrated area, the 
latter's dulness will be demonstrable. Neither light nor strong per- 
cussion may avail in eliciting the dulness of diffuse disseminated 
areas of infiltration, owing to the prevailing resonance of the sur- 
rounding pulmonary tissue, whereby the dulness is so effectually 



146 



PHYSICAL DIAGNOSIS 



masked that it escapes notice. This is particularly true if strong 
percussion be made, for the more forcible the blow, the more intense 
the vesicular vibrations. Analogous to this is the neutralization of 
dulness from consolidation by the undue resonance of the adjacent 
relaxed or vicariously distended lung*. 

The situation of a jiull or a flat area has a certain clinical bearing 
upon the character of the underlying lesion, although deductions 



Consolidation. 



Light Percussion 
(nesonance) 




Consolidation. 



Strong Tireussion 



(Impaired. 
Resonance) 



Light Percussion 
/pulnessj (§jE 



&$$:. Consolidation 




Percussion 



(Impaired 
Resonance) 




The effects of variable percussion force. 



based upon such a premise are to be made only in correlation with 
other physical signs. Thus, apical impairment of the percussion sound 
is most suggestive of tuberculosis; equality of the sound at both apices 
points to an incipient left-sided infiltration, since in health the upper 
right lobe shows relative impairment. (Seep. 128.) A second important 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 147 

factor of apical dulness is the so-called apex pneumonia, which occurs 
especially in children. Sternal and parasternal dulness, generally 
near Louis' angle, is found in mediastinal tumors large enough to 
have encroached anteriorly upon the inner surface of the sternum, 
and laterally upon the anterior borders of the lungs. The dulness 
of tumors of the lungs and the pleura cannot be referred definitely 
to any distinct topographic region. Dulness or flatness at the base 
posteriorly, if not obviously due to enlargement of the. liver or the 
spleen, is commonly a sign of croupous pneiynonia, fluid within the 
pleural cavity, and pulmonary edema, infarction, or hypostatic con- 
gestion. Basal flatness shifting with the subject's change of posture 
occurs in pleural transudates, such as hydrothorax and hemothorax; 
rarely, if ever, does an inflammatory pleural exudate gravitate in 
this manner. Paravertebral dulness, if bilateral, should prompt a 
search for atelectasis and its exciting factors, or for hydrothorax; if 
unilateral and right-sided, hilus tuberculosis is suggested (Philippi) . 
In pleural effusion a triangular patch of paravertebral dulness above 
the level of the twelfth rib may be demonstrable on the unaffected 
side — Grocco's sign. (See p. 280.) Impairment in the interscap- 
ular area is significant of enlargement of the bronchial glands, as 
well as of aneurism of the descending aorta, which causes dulness 
between the vertebral column and the left scapula. Dulling of the 
normal tympany in Traube's space may be due to fluid within the 
left pleural sac, and to enlargements of the heart, liver, or spleen, 
while in pericardial effusion, adhesive pericarditis, right pleural effu- 
sion, pleural thickening, and basal pneumonia the normal resonance 
of Ebstein's cardiohepatic angle may be obliterated. Dulness in the 
axilla is commonly a sign of pulmonary infarction. 

Unilateral dulness, of a peculiar wooden quality, over the greater 
part of one lung, is often met with in pulmonary cirrhosis, and mul- 
tiple patches of impaired resonance are sometimes to be detected in 
catarrhal pneumonia, miliary tuberculosis, and pulmonary syphilis. 

Hyper resonance and Tympany. — Exaggeration of pulmonary 
resonance indicates that the structures within the percussion sphere 
contain an abnormally large volume of air, that their mural tension 
is altered, or that they conduct clearly the hyperresonance of adjacent 
air-containing parts, according to the character of the exciting cause 
of the altered sound. Thus, hyperresonance is met with as the result 
of vesicular emphysema, bronchopulmonary cavities, pneumothorax, 
parabronchial consolidations, and pulmonary relaxation consequent 
to mechanical or to parenchymatous changes (Fig. 83). 



148 



PHYSICAL DIAGNOSIS 



The increased resonance of hypertrophic emphysema, dubbed 
"band-box resonance," is explained by the unduly excessive volume 
of air within the lungs, and by the state of pulmonary relaxation due 
to permanent overdistention and destruction of the alveolar tissue. 
In the condition termed compensatory emphysema hyperresonance 
is elicited over the lung vicariously dilated in consequence of crippling 
of the opposite lung. The exaggerated resonance expressive of these 
emphysematous changes is a commingling of the vesicular and the 
tympanitic qualities, of abnormally increased intensity and duration, 
and of a pitch rising in proportion to the predominance of the tym- 
panitic quality — the vesiculotympanitic resonance of Flint. Acoustic - 



Craoked-p 
Tympany 



Tymbcuty 



erresonance. 




Tympany 



Fig. 83. — The effect of pulmonary cavities, pneumothorax, and emphysema upon 
the percussion sound. 



ally, this sound is essentially similar to the resonance of Skoda, 
described below. 

Pulmonary hyperresonance commonly accompanies the extremes 
of life— as in the young child, whose lungs, owing to their great 
elasticity, are prone to temporary dilatation from simple respira- 
tory overaction, as, for example, during a fit of crying; and in the 
very aged, whose lungs, in consequence of senile changes, are in a 
state of relaxation. In scoliosis circumscribed patches of compensa- 
tory hyperresonance may be found opposite to the vertebral con- 
vexity (Gray). 

Conditions of pulmonary relaxation secondary to compression and 
to parenchymatous disease of the lungs may account for a decided 






EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 49 

increase in the resonance of the percussion sound, owing to the 
diminished tension of the vesicular tissues. This sort of hyper- 
resonance, termed Skodaic resonance, is elicited by percussion over 
the compressed lung immediately above a pleural effusion or an 
extensive basal pneumonia; less readily it can be detected over the 
relaxed pulmonary tissue adjacent to an intrathoracic neoplasm, an 
enlarged heart, or a large pericardial effusion. Upward displace- 
ment of the diaphragm, secondary to excessive intra-abdominal 
pressure, crowds the lungs upward and lowers their tension to a 
degree provocative of greatly exaggerated resonance. In the for- 
mative stage of obstruction atelectasis hyperresonance is found over 
the area corresponding to the patch of airless relaxed lung. In 
acute febrile states a general hyperresonance, presumably due to 
diminished pulmonary tension of toxic origin, has been described 
by Samuel West as an " acute pulmonary tympanites." 

Hyperresonance dependent upon parenchymatous changes in the 
lungs develops in the congestive stage of croupous pneumonia, in 
pulmonary edema, and in pulmonary infarction, all of which lesions 
lower the tension of the vesicular structure. 

It should be borne in mind that the hyperresonance observed in 
the foregoing conditions is incidental only to the stage of pulmonary 
relaxation, for when the affected lung becomes consolidated, dulness 
at once appears. This transition from hyperresonance to dulness 
occurs, for example, in compression atelectasis so soon as the vesicular 
structure becomes infiltrated or carnified, and in croupous pneumonia 
when the stage of red hepatization sets in. 

Pulmonary and bronchiectatic cavities, inasmuch as they act as 
air-containing resonating chambers, furnish a tympanitic percussion 
sound whose tonal characteristics vary with the physical properties 
of the excavation and the adjacent parts. It is important to under- 
stand that a cavity affords typical physical signs only when it is super- 
ficial, filled with air, and resilient, with a free bronchial outlet. A 
large cavity may be so deeply buried in the parenchyma of the lung 
as to escape recognition, even by the most vigorous percussion; while 
a much smaller cavity, if it be superficial, can generally be detected 
by gentle percussion. When the air within a cavity is replaced by 
liquid, the primary tympany changes to flatness, which becomes more 
and more marked as the resonating chamber of the cavity is thus 
abolished. Should the cavity be emptied by expectoration, the 
primary tympany reappears, and a similar transition from tympany 
to flatness to tympany may occur as the result of the lodgment and 



150 PHYSICAL DIAGNOSIS 

the dislodgment of a tight mucous plug in the cavity's bronchial 
outlet. The mural resiliency of a cavity is also an important deter- 
mining factor in the character of the tympanitic sound: in two cavities 
of equal size, the one having the more relaxed walls affords the lower 
pitched and intenser sound. It is common to find a dull undertone 
to the tympany over- a pulmonary cavity adjacent to a patch of pul- 
monary infiltration or of pleural thickening (Fig. 83). 

Over a pneumothorax, or an effusion of air within the pleural 
sac, loud tympany, perhaps of a metallic tone, is heard on 
percussion, provided that the mural tension is not excessive. If 
this be so, the percussion sound, although unnaturally intense, is 
dull and muffled and toneless. Pneumothoracic tympany frequently 
extends far beyond the anterior and the inferior borders of the lung, 
owing to the tendency of the air to fill the complementary pleural 
sinus. Therefore, the tympany encroaches upon the dull areas 
overlying the heart, the liver, and the spleen, from whichever quarter 
the effusion spreads. Upward extension of the hyperresonance also 
takes place, for the lung above a pneumothorax is relaxed by the 
upward pressure of the intrapleural air: in the extreme instance the 
entire side of the chest emits an intensely tympanitic percussion sound. 
Since a pneumothorax eventually excites pleural effusion into the 
air-distended sac, the tympanitic area sooner or later is underl'aid 
by a zone of flatness, which, unlike the flatness of a simple inflam- 
matory exudate, shifts with the subject's change of position 
(Fig. 81). 

Parabronchial consolidations conduct the normal percussion 
tympany of the large bronchi and the trachea, tympany from this 
cause being demonstrable by percussing over tuberculous and pneu- 
monic consolidations lying between the larger bronchi and the inner 
surface of the thorax (Fig. 81). 

Amphoric Resonance . — This is a variety of tympany characterized 
by a prolonged empty, echoing sound of high pitch and distinctive 
metallic quality. It may be fairly well imitated by flapping the 
cheek with the finger when the mouth is closed and moderately dis- 
tended with air, or by tapping the side of an empty jar — hence the 
term, "jug sound." 

Amphoric resonance may be demonstrated by forcible percussion 
over an air-containing cavity of fair size and superficial situation, 
with smooth, thin, moderately tense walls, and a small outlet, or 
none at all. Pneumothorax and tuberculous cavities occasionally, 
though by no means frequently, afford tympany of this peculiar 
echoing character. 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 151 

Cracked-pot Resonance. — This form of tympany is recognized 
by its distinctive chinking quality, which has been likened to the 
muffled chink of coins (money-chink resonance), and to the sound 
produced by striking the side of a cracked metal jar (cracked-pot 
sound; bruit de pot fele) . This sound may be counterfeited by clasping 
the hands so as to form a cavity, and striking them sharply against 
the knee, thus suddenly expelling, with an audible " chink," a jet 
of air through the constricted orifice between the opposed palms. 
The essential element of the cracked-pot sound is the sudden expul- 
sion of air from a cavity through a small opening, and this noise 
blends with the ordinary tympany of the cavity to produce the char- 
acteristic sharp "chink." To elicit the sign, strong percussion should 
be made during expiration, the patient's mouth being open when the 
blow is struck. 

Interpreted in connection with other physical signs, the cracked- 
pot sound is an important indication of a cavity, but as a single 
isolated rinding, it is of most uncertain utility. It is to be heard, 
especially at an apex, over a superficial cavity with tense, though 
resilient, walls, and a free bronchial outlet, and at the base over 
a pneumothorax communicating with the air by a fistula leading 
either into a bronchus or through the chest- wall (Fig. 83). The 
sound is also sometimes elicited over an acutely congested lung, as 
well as over the relaxed, compressed pulmonary tissue above the 
upper level of a pleural effusion. A highly resilient normal chest, 
if percussed with considerable force, may emit a spurious cracked- 
pot sound, produced by the rush of the escaping air plus the loud 
sound of pulmonary resonance. It is not uncommon to find this 
in the young child, particularly during the act of crying, which, 
by narrowing the glottis, impedes the egress of the air-columns 
set in motion by the percussion blow. As already pointed out, a 
cracked-pot sound may be closely imitated should the pleximeter 
finger not be closely applied to the surface of the chest when the 
percussion blow is delivered. 

Special Tonal Changes of the Percussion Sound. — Several 
distinctive alterations in the pitch, intensity, quality, and permanence 
of the percussion sound have been described as aids in determining 
not only the initial diagnosis of solid and hollow pulmonary lesions, 
but also, in the case of the latter, in gaging the size and the shape of 
the cavity, the amount of its contained fluid, and the patency of its 
communication with the external air. 

Wintrich's Sign. — Percussion over a cavity gives clearer, louder. 



152 



PHYSICAL DIAGNOSIS 



and higher pitched tympany when the patient's mouth is open than 
when it is closed. This change of note, known as Wintrich's sign, 
is found over superficial cavities and over pneumothorax, in either 
of which conditions a free bronchial communication is essential for 
its production, the mechanism of which consists in the transmission 
of the percussion vibrations to the tracheal air-columns, and thence 





— Wintrich's interrupted change of note. 



to the mouth, where they are amplified and resonated by the action 
of the pharynx. In eliciting Wintrich's change of note the examiner's 
ear should be kept directly beneath the open mouth of the patient, 
who is instructed to elevate the chin, to protrude the tongue, and to 
inspire forcibly, even beyond the ordinary acme of inspiratory excur- 
sion. The sign can be fairly well imitated by percussing over the 
trachea, first with the subject's lips tightly closed and then with them 
wide agape. 

If Wintrich's sign appears and disappears, depending upon the 
posture of the patient's body, the change is termed Wintrich's inter- 
rupted change of note. This sign indicates a cavity containing fluid, 
which shifts as the subject changes his position, so that, the bronchial 
outlet is alternately occluded and left unobstructed (Fig. 84). 

Williams' Tracheal Tone. — Percussion over an infiltrated or a com- 
pressed apical lesion may show an alteration of note similar to that 
of Wintrich, the sound changing from dulness, when the patient's 
mouth is closed, to clear high-pitched tracheal tympany when the 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 53 

mouth is open — the tracheal tone of Williams. An analogous tonal 
alteration has been found by Hoover when the upper part of the 
sternum is percussed in cases of anterior mediastinal new-growth, 
aneurism of the ascending aortic arch, and large pericardial effusion; 
and, according to Grober, tympany with a Wintrich tone change is 
demonstrable in tumors of the posterior mediastinal space. The 
production of Williams' tracheal tone in the foregoing lesions depends 





Low-pitched tympany with subject erect. High-pitched tympany with subject recumbent. 

Fig. 85. — Gerhardt's sign. 



upon the transmission of the percussion waves to the trachea, whose 
air-columns, thus agitated, lend a tracheal quality to the sound 
primarily excited in the area percussed. 

Friedreich's Sign. — Inspiratory elevation and expiratory lowering 
of the pitch of cavity tympany is known as Friedreich' 's sign, which 
requires for its production physic c 1 conditions identical with those 
responsible for Wintrich 's change of note. Respiratory change of 
pitch is attributed to variations in the mural tension of the cavity 
and in the size of the chink of the glottis, which occur with the act 
of breathing. Unless associated with other more definite indications 
of a cavity, Friedreich's sign is likely to be misleading — a similar 
respiratory change of pitch, differing from it chiefly in degree, may 
be readily demonstrated by vigorous percussion over the normal 
lungs, owing to differences in pulmonary tension during inspiration 
and expiration. (Cf. Adherent Pericardium.) 



i54 



PHYSICAL DIAGNOSIS 



Gerhardt's Sign. — This is a change of note relating to the shape of 
a pulmonary cavity, and consists of an alteration in the pitch of the 
percussion tympany, occurring when the patient's posture is changed. 
In order to afford this change of pitch a cavity must be partly rilled 
with fluid, have unequal axes, and have an unobstructed bronchial 
outlet. Under these circumstances the pitch of the tympany is 
lower when the long axis of the cavity is horizontal than when 
it is vertical (Fig. 85). Thus, a cavity with a long horizontal 
axis emits a lower tympany when the patient sits erect than when 
he lies upon the back, while one with a long vertical axis affords 

higher pitched tympany under 
the same conditions of pos- 
ture. An identical change of 
pitch, known as Biermefs sign, 
may be elicited over a hydro- 
pneumothorax, in which con- 
dition the percussion tympany 
is low pitched when the patient 
is recumbent and high pitched 
when he is erect, since in re- 
cumbency the long horizontal 
axis of the pleural cavity is 
increased by the gravitation of 
the fluid. Of these two signs, 
Biermer's is the more constant. 
This is so because the pleural 
cavity more readily provides 
Fig. 86.— Mechanism of bell tympany. tne necessary acoustic condi- 
tions than a pulmonary excava- 
tion — the former frequently serves as a simple oval resonating 
chamber, while the latter is ordinarily of exceedingly irregular shape, 
with several axes of unequal length. 

Bell Tympany. — In pneumothorax a distinctive metallic echo 
(bruit d'airairi) may be elicited by a special sort of auscultatory 
percussion known as Gairdner's coin- test (Fig. 86). This consists 
of auscultating over the lower thorax posteriorly, while an assistant 
percusses at the same level anteriorly, using the edge of one large 
silver coin as a plexor and the flat surface of another as a pleximeter. 
If the pleural sac be filled with air, the impact of the two coins is 
heard as an echoing metallic ring, not unlike the distant sound of a 
hammer and anvil or of a chime of bells. It is also possible to hear 




EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 55 

the bell sound over a large, empty, superficial pulmonary cavity 
having the resonating properties of a pneumothorax. 

Here may be mentioned the transmission of the metallic click of 
two coins, demonstrable by the above technic in pleural effusions 
(Pitres's signe du sou). This sound, however, wholly lacks the 
chiming tone so typical of pneumothorax, being harder, more 
"chinky," and less echoing. The tone is simply dull when fluid 
and consolidation coexist. 

The Lung Reflex. — Not infrequently a circumscribed area of pul- 
monary resonance becomes decidedly hyperresonant after prolonged 
and vigorous percussion, this alteration of sound being ascribed to a 
temporary dilatation of the lung, excited reflexly, beneath the part 
percussed. Abrams has described, under the term lung reflex, this 
sort of circumscribed hyperresonance resulting from local irritation 
of the surface of the chest by the application of heat, cold, friction, 
and mustard, which apparently provokes dilatation of the vesicular 
tissue beneath the irritated surface area. 

AUSCULTATION OF THE LUNGS 

Auscultation is the means of studying the normal respiratory 
sounds and their pathologic modifications, of judging the character of 
the voice resonance, and of detecting sundry adventitious sounds 
produced in the bronchopulmonary structures and in the pleura. 
Either the mediate or the immediate method may be employed, 
according to the examiner's preference — there are those who believe 
that poorly denned chest signs, such as very fine crepitations and 
distant pathologic breathing, can be detected most easily by applying 
the ear directly to the chest, and there are those who,, accustomed to 
using a stethoscope, can judge respiratory sounds most accurately with 
this instrument. The exceptional instances in which the naked ear 
serves better than the stethoscope have been referred to in the pre- 
ceding section. (See p. 23.) 

To obtain trustworthy results, the patient should breathe regularly, 
tranquilly, and somewhat more deeply than normal, thus fully inflat- 
ing and deflating the lungs, while the examiner auscultates systemati- 
cally over the different areas within the pulmonary borders. The 
sounds thus elicited are analyzed and compared with those afforded 
by deeper, more forcible respiration, which in some instances is 
necessary to develop tangible findings. To avoid the production 
of extraneous noises within the upper air-passages, the patient is 



i56 



PHYSICAL DIAGNOSIS 



instructed to breathe with the mouth partly open, the cheeks and 
nares being relaxed, and to guard against forcible, noisy respiration. 
These essential precautions, though of themselves simple, are not 
easy to put in force, for the average subject is not readily taught 
how to breathe properly. 

THE RESPIRATORY SOUNDS 

The respiratory sounds audible over the normal thorax conform 
to two principal types, vesicular and bronchial, to which may be 
added, for convenience sake, a subsidiary variety, which combines 
the characteristics of both, the bronchovesicular. Each of these 
types of breathing is audible, in health, only in certain definite 
regions of the chest, and, this being so, the substitution of one 







Normal. 



Puerile. 



Senile. 



Harsh. 



Expiration 






Bronchial. Bronchovesicular. Wavy. Cog-wheel. 

Fig. 87. — Normal and pathologic types of the respiratory murmur. 

respiratory type by another (such as the existence of bronchial or 
of bronchovesicular breathing in a region normally affording a pure 
vesicular sound) is to be regarded as pathologic. 

Vesicular Breathing. — The normal vesicular murmur is a soft, 
rustling, breezy, low-pitched sound, whose inspiratory and expira- 
tory cycles blend so imperceptibly that no distinct interval of silence 
separates them (Fig. 87). The inspiratory phase best illustrates the 
distinctive breeziness, the low pitch, and the moderate intensity of the 
sound, for during the expiratory phase the quality is a trifle harder 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 57 

and more blowing, the pitch higher, 1 and the intensity decidedly 
less — in fact, the expiratory sound may be so weakened that it is prac- 
tically inaudible. The ratio of the inspiratory to the expiratory sound 
is 3:1. Normal vesicular breathing may be imitated with toler- 
able accuracy by breathing naturally with the lips held in the position 
of pronouncing the letter/. It may be heard in its typical character 
over the left infraclavicular, the infrascapular, and the axillary regions, 
where only alveolar tissue lies directly beneath the auscultator's ear. 

To account for the origin of the vesicular murmur several theories 
have been suggested, no one of which appears to be wholly adequate. 
Baas' theory assumes that the sound is merely a modification of the 
blowing sounds of the larynx and the trachea, which become softened, 
muffled, and otherwise altered by their conduction through the 
bronchopulmonary structures. But, according to Sahli, the local 
movements of the pulmonary parenchyma also account for certain 
elements of the vesicular sound. Together, these two hypotheses 
serve as a better explanation than the original theory of Laennec, 
that the sound was due to the friction of the air-currents in the bron- 
chioles and the infundibula, or than Bueri's hypothesis of the im- 
pact of central and peripheral air-columns. 

Bronchial Breathing. — Bronchial breathing is distinguished by 
its loud, blowing, tubular quality, high pitch, and the distinct interval 
of silence which separates inspiration and expiration (Fig. 87). Of 
the two breath-sounds, expiration is generally more intense, higher 
pitched, and more distinctively tubular. The duration of the respira- 
tory phases is about equal, if, indeed, expiration is not decidedly the 
longer, and neither carries even the faintest trace of that soft, quiet 
breeziness peculiar to the normal vesicular murmur. The bronchial 
respiratory sound may be elicited in the healthy adult by ausculta- 
tion in those areas of the thorax lying directly over the larynx and 
the trachea — the suprasternal notch, the upper sternal region, and 
the lower cervical vertebrae. As Barach points out, both bronchia) 
respiration and bronchophony are audible at the acromial end of 
the clavicles, owing to the excellent conducting properties of 
these bones. The bronchial tone may be counterfeited by breath- 
ing deeply with the mouth fixed, so as to pronounce the syllable 
"hu" or the consonant " ch." 

Bronchial breathing is merely the unmodified sound of the laryn- 
gotracheal murmur, which is a glottidean tone due to the passage 
of air-columns, during inspiration and expiration, through the glottis 

1 The truth of this statement, originally made by Austin Flint, in 1852, must 
be apparent to one that judges sound by intelligent auscultation, despite the 
view expressed by some that the pitch of expiration is lower than that of inspira- 
tion. 



158 PHYSICAL DIAGNOSIS 

into the wider caliber of the windpipe above and below, with the 
consequent production of air-eddies and their reflection both up- 
ward toward the pharynx and downward through the trachea and 
the' larger bronchial tubes. 

The detection of bronchial breathing over areas of the lung to 
which this sound is foreign signifies that in such areas the vesicular 
structure is in a condition of infiltration, compression, or excavation, 
in consequence of which the bronchial tone, normally enfeebled by 
healthy pulmonary tissue, is conducted to the surface of the chest 
with unimpaired intensity and quality. This type of respiration, 
therefore, is met with in pneumonic and tuberculous consolidations; 
in pulmonary and bronchiectatic cavities with a free bronchial out- 
let; and in pulmonary compression and collapse secondary to pleural 
effusion, neoplasm, and aneurism. (See Figs. 81 and 83.) Other 
conditions that account for bronchial respiration are edema, abscess, 
gangrene, infarction, cirrhosis, syphilis, cancer, and actinomycosis. 
A mass of enlarged bronchial glands or a mediastinal neoplasm 
situated in intimate relation with the larger air-tubes and the thoracic 
parietes may distinctly transmit to the latter the bronchial tone. 

Full respirations are essential to bring out all the characteristics 
of bronchial breathing, as can be demonstrated by auscultating 
over a consolidation, while the subject takes alternately shallow 
and deep breaths. 

Cavernous and amphoric breathing are two subvarieties of 
bronchial respiration, distinguished by certain peculiarities in their 
quality and pitch. Cavernous breathing is distinguished by its deep 
and hollow quality, low pitch, and usually, but not invariably, by 
the fact that expiration is of lower pitch than inspiration. A super- 
ficial cavity with resilient walls and a patent bronchial outlet is the 
usual factor of this sort of breathing, such a cavity being either 
pulmonary or bronchiectatic, and due to tuberculosis, abscess, or 
gangrene. The proximity of an area of infiltration to the excavation 
may add to the cavernous tone a high-pitched tubular bronchial 
quality during expiration, and to this modification Flint has applied 
the term bronchocavernous respiration. A patch of healthy lung 
surrounding a cavity may ingraft its vesicular quality upon the 
cavernous sound, and thus produce a hybrid type of breathing known 
as vesiculocavernous. The distinctions between these two sub- 
varieties of cavernous breathing, though hypothetically plausible, 
are too finely drawn to be appreciated save by one who possesses a 
most cultivated sense of acoustics. 

Amphoric breathing is recognized by its characteristic musical, 
metallic, echoing quality, which replaces the hollow tone of pure 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 59 

cavernous and the tubular blowing of typical bronchial respiration. 
The sound produced by blowing gently into the mouth of an empty 
vessel closely imitates the musical quality of amphoric breathing, 
which is the auscultatory complement of the amphoric percussion- 
note and of the bell-tympany elicited over pneumothoracic and 
large pulmonary cavities. The pitch of the foregoing types of breath- 
ing depends chiefly upon the size of the cavity, being higher the 
smaller the size of the resonating chamber, and vice versa. 

A minor subvariety of bronchial breathing, known as Seitz meta- 
morphosing respiration, is distinguished by an inspiratory murmur 
beginning as a tubular bronchial sound, and ending as either a caver- 
nous or an amphoric tone. Less commonly, this change of quality 
affects expiration or both respiratory phases. This bronchocaver- 
nous breath-sound is afforded by a cavity having a small patent 
bronchial outlet. Over tuberculous infiltrations there is sometimes 
to be heard a type of breathing beginning as a vesicular and ending 
as a bronchial or bronchovesicular sound — the " veiled puff" ("souffle 
viole*") of Laennec. 

Bronchovesicular Breathing. — This type of respiration, as its 
name suggests, is a mixture of the bronchial and vesicular murmurs, 
such as may be heard in those areas of the normal thorax where the 
range of auscultation includes the sounds of both the large bronchi 
and the vesicular structure. It is audible, therefore, over and along- 
side the sternum at the level of Louis' angle, and over the inter- 
scapular spaces on each side of the spine, at the level of the third or 
fourth thoracic vertebra, these being the situations where the primary 
bronchi, covered by an intervening layer of vesicular tissue, lie close 
to the surface of the chest. The sound is louder and decidedly more 
bronchial in tone on the right side, owing to the anatomic peculiarities 
of the right bronchus. 

The inspiratory phase of bronchovesicular breathing is purely 
vesicular, or, less commonly, tinged with a bronchial tone, while 
expiration is of a more bronchial character. Expiration is as 
long as, if not longer than, inspiration, which, aside from its 
shorter duration, is the quieter and the lower pitched of the two 
sounds. No matter what be its finer acoustic variations, — and their 
number is legion, — so long as respiration affords this blending of the 
bronchial and vesicular sounds, the term bronchovesicular is applic- 
able, or, if one chooses, a synonymous adjective like rude, sub- 
tubular, indeterminate, or transition (Fig. 87). 

Pathologically, bronchovesicular breathing occurs as the result 
of pulmonary lesions that conduct the bronchial tone to the surface 
of the chest, along with more or less of the normal vesicular murmur 



l6o PHYSICAL DIAGNOSIS 

(Fig. 81). This acoustic condition is fulfilled by small, disseminated 
consolidations separated by unimplicated vesicular structure, as in 
catarrhal pneumonia and incipient phthisis; by a large area of con- 
solidation or excavation adjacent to healthy lung, as in central crou- 
pous pneumonia, tuberculous infiltration, and pulmonary or bronchi- 
ectatic cavities overlaid by normal pulmonary tissue; by an area of 
compressed, atelectatic lung, such as the zone of pressure atelectasis 
lying directly above a pleural effusion. The bronchial element of 
bronchovesicular breathing may diminish or disappear, should the 
bronchial tube communicating with the infiltrated or excavated patch 
be obstructed by secretion, while the vesicular element may be 
similarly modified, should the tube leading to the healthy vesicular 
area be blocked. Bronchovesicular respiration is especially signifi- 
cant of some pathologic factor when it is elicited over parts of the 
lungs well removed from the normal sites of this type of breathing, 
but these areas are by no means exempt from consolidative processes. 

Prolonged Harsh Expiration. — Reversal of the inspiratory- 
expiratory ratio, with harshness and impurity of the expiratory 
sound, denotes some impediment to the free egress of the broncho- 
pulmonary air-columns during the act of breathing, and, in general 
terms, it may be stated that the greater this interference, the more 
decided the impurity and the lengthening of the sound (Fig. 87). 
At the left apex prolonged high-pitched expiration is exceedingly 
suggestive of tuberculous infiltration, while a prolonged low-pitched 
expiratory sound, audible over the greater part of both lungs, is 
found in the chronic bronchitides of emphysema and asthma. 
Undue prolongation and harshness of the expiratory murmur is to 
be expected as a physiologic sign over the upper part of the right 
lung. 

Puerile or Exaggerated Breathing. — An exaggeration in the 
intensity of the vesicular murmur is known as exaggerated, harsh, 
rough, or puerile breathing. This type of respiration is physiologic 
in children below the age of puberty, being more pronounced the 
younger the child; in the healthy adult it is audible above and below 
the right clavicle, and frequently also at the left base posteriorly 
(Cabot) . A thin, elastic chest-wall magnifies the vesicular murmur, 
perhaps to the degree of puerility, while a thick, rigid chest blocks 
the transmission of the sound. 

Pathologically, puerile breathing is elicited over a lung that is 
variously overacting in consequence of crippling of the opposite 
lung by a wide-spread congestion, infiltration, effusion, or neoplasm; 
or over a circumscribed portion of a lung that is overworked, so as 
to compensate for a lesion elsewhere in the same lung. Catarrhal 






EXAMINATION OF THE BRONCHOPULMONARY SYSTEM l6l 

obstruction of the smaller bronchi is a most important cause of harsh, 
rough breathing, owing to the stenotic interference with the move- 
ments of the bronchiolar air-columns attending this affection. Dysp- 
neic overaction of the lungs, such as that incident to active muscular 
exertion or to uncompensated cardiac disease, may also account 
for abnormal intensity and harshness of the breath-sounds. 

Puerile and bronchovesicular breathing are, superficially, not 
unlike, but they differ in that the former, though loud and harsh, is 
untainted by the bronchial tubular tone and is not attended by any 
disturbance in the normal inspiratory-expiratory ratio. These dif- 
ferences also serve to differentiate bronchial breathing, should it 
prove a source of confusion. 

Senile or Feeble Breathing (Fig. 87). — Enfeeblement of the vesic- 
ular murmur, or senile breathing, is common in the aged and in states, 
of asthenia and debility, as the result of defective pulmonary resiliency 
and of weak respiratory movements. Normal lungs may emit 
suppressed, distant sounds simply because the subject breathes so 
quietly that the vesicles are improperly inflated with inspiration. 

In disease a senile type of breathing is symptomatic of many differ- 
ent conditions relating to defective distention of the pulmonary 
alveoli and to the non-conduction of the normal pulmonary murmur. 
In paralysis of the respiratory muscles and in painful affections, such 
as acute pleurisy, pleurodynia, and trauma of the chest, it is natural to 
expect suppressed, quiet breathing, because of the limited thoracic 
expansion. In bronchial obstruction, as by foreign body, pressure, 
or secretion, diminution of the respiratory murmur is elicited over that 
part of the pulmonary parenchyma supplied by the stenotic tube, the 
general rule holding true that the higher the location of the obstruc- 
tion, the larger the area of enfeebled sound. Imperfect vesicular 
distention, weakening the breath-sounds, may occur in chronic adhe- 
sive pleurisy, owing to restriction of the pulmonary excursions by 
dense fibrous bands; in hypertrophic emphysema, because of the 
rigid, overinflated condition of the vesicles; in the first stage of 
croupous pneumonia, when the lungs are engorged and fixed and 
abnormally tense; in atelectasis (due to either obstruction or com- 
pression) for the reason that the affected area receives no air supply 
and is too relaxed to vibrate. In disseminated tuberculous infiltra- 
tion the respiratory sounds may be weakened as the result of hyper- 
tension of the non-tuberculous portions of the lungs and from cir- 
cumscribed catarrhal stenosis of the small bronchi (Sahli), though 
more commonly this type of infiltration is betrayed by broncho- 
vesicular or by harsh, impure breathing. The respiratory sounds are 



1 62 PHYSICAL DIAGNOSIS 

suppressed in some cases of active congestion, edema, and cirrhosis 
of the lungs, and in those forms of massive pneumonia in which 
a fibrinous exudate blocks a large part of the bronchial lumen. 

Enfeeblement of the respiratory sounds, by fault of their poor 
conduction to the surface, is found when a liquid or a solid media is 
interposed between i;he lungs and the chest-wall. The sound is 
damped in this manner by extensive pleural effusions, by pleural 
thickening, and by intrathoracic new-growths not continuous with the 
pleuropulmonary surfaces. In pneumothorax the breath-sounds 
become weak and indistinct when the bronchial outlet of the cavity 
is obstructed. 

Absent Breathing. — Total suppression of the respiratory murmur 
occurs as the result of any change acting as an effectual barrier to 
the conduction of bronchopulmonary sounds to the surface of the 
chest. Any factor of senile breathing, therefore, may altogether sup- 
press the breath-sounds, should it produce the essential acoustic 
conditions of such a change. The most important causes of totally 
absent breath-sounds are pleural exudates and transudates, bronchial 
and bronchiolar obstruction, closed pneumothorax, and pulmonary 
cavities filled with liquid — conditions which, it is obvious, may 
block all sound vibrations at some point between their origin in the 
glottis and the surface of the thorax (Fig. 81). 

Cog-wheel or Interrupted Breathing. — In this type of breathing 
the inspiratory murmur is interrupted by a series of short, jerky 
pauses, or it is composed of a succession of undulatory, wavy sound 
modulations; less commonly these peculiarities are audible during 
expiration. More or less exaggeration and impurity of the whole 
vesicular murmur frequently accompanies the foregoing changes, 
although they may also be attended by suppression of the breath- 
sounds (Fig. 87). 

Circumscribed cog-wheel breathing indicates catarrh of the finer 
bronchi, with obstruction to the free movements of the bronchiolar 
air-columns and irregular inflation and deflation of the lobules 
supplied by the inflamed tubes. This change is commonly found 
in early phthisis, of which cog-wheel respiration (especially if localized 
at the apex)" is a most suggestive physical sign. Generalized cog-wheel 
breathing over the whole thorax is due simply to intermittent con- 
tractions of the respiratory muscles, and it means, therefore, nothing 
more serious than fatigue, nervousness, chest pain, or perhaps incom- 
plete paralysis of the muscles concerned in breathing. 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 63 



VOCAL RESONANCE 

Vocal or voice resonance, which bears the same relation to auscul- 
tation as does vocal fremitus to palpation, has the same physical 
origin as its tactile equivalent, and is modified by pathologic proc- 
esses identical with those that influence the latter. The audible 
and tactile fremitus, then, correspond, under both normal and abnormal 
conditions, and hence are corroborative in the study of the laryngo- 
tracheal voice vibrations by the senses of touch and of hearing. 

In eliciting vocal resonance the stethoscope should be placed over 
a region of the chest not immediately adjacent to the main bronchial 
tree, while the patient repeats "ninety-nine" or "one, two, three," 
with his lips turned away from the auscultator's ear. Normal 
vocal resonance sounds like a confused, buzzing hum that carries 
no trace of articulate sound — it is merely an indistinct, far-away 
vibration, which seemingly arises within the depths of the thorax, 
and never conveys to the examiner the clean-cut, sharp pronuncia- 
tion of the words uttered by the speaker. Auscultation just above 
the lower pulmonary borders typically illustrates these peculiarities 
of the sound. The resonance of the voice, like its fremitus, is normally 
•exaggerated over the site of the large air-passages, and is modified 
by the pitch and intensity of the subject's voice and by the conducting 
qualities of the thoracic parietes. 

Increased Vocal Resonance. — As a pathologic change, increase 
in the intensity of the voice resonance depends upon pulmonary 
infiltration, excavation, or compression, and upon bronchiectatic 
cavities, the several underlying causes of which have already been 
enumerated (Fig. 81). Bronchophony, or the bronchial voice, is 
the term used to express an exaggeration of vocal resonance so 
striking that it seems as if it were produced just beneath the chest- 
wall, though, in spite of its intensity, bronchophony invariably remains 
a confused, inarticulate rumble. Normally, this bronchial sound 
is audible over the course of the trachea and primary bronchi. Pec- 
toriloquy, a refinement of bronchophony, is the transmission of 
articulate speech to the surface of the thorax, where not only the spoken 
words, but also their syllables, are heard with a clear, distinct inten- 
sity. Whispering pectoriloquy, or the conduction of the articulate 
whisper through the chest-wall, is a still greater refinement of bron- 
chophony, and stands for the acme of increased vocal resonance, 
in which the sound conduction is exquisitely developed. Pectoriloquy, 
either spoken or whispering, is most suggestive of a cavity, but it is 
not restricted to such a lesion, as Laennec believed, since it is not 



164 PHYSICAL DIAGNOSIS 

infrequently audible over an area of pulmonary infiltration or com- 
pression. Page proposes the word bronchiloquy to express the high- 
pitched pectoriloquy due to a consolidated lung, and the term cavern- 
iloquy, for the low-pitched pectoriloquy afforded by a cavity, while 
he designates as amphoriloquy the intense amphoric voice-sounds 
which correspond to the amphoric percussion-note and respiration. 
Egophony is a form of bronchophony characterized by a peculiar 
quavering nasal tone, comparable to the bleating of a goat. This 
sign, whose mechanism is not understood, is sometimes heard just 
above the upper level of a pleural effusion, and also above various 
pulmonary infiltrations. Its clinical significance does not differ from 
that of the ordinary bronchial voice. 

BaccdlVs sign, or the transmission of whispering pectoriloquy 
through a serous, but not through a purulent, pleural effusion has 
been used as a point of differentiation between these two conditions, 
but on insufficient grounds, for though absent over an empyema, 
the whispered voice is also inaudible over many serous effusions of 
large volume. 

Decreased Vocal Resonance. — Enfeebled, sometimes absent, voice 
resonance is to be expected as the result of emphysema, bronchial 
occlusion, thickened pleura, pleural effusions, and the other causes 
of diminished tactile fremitus referred to in a preceding section. 
(See p. 136.) 

ADVENTITIOUS SOUNDS 

In addition to the several modifications of the vesicular murmur just 
described, certain superadded, foreign sounds arise in consequence 
of pathologic changes affecting the bronchial tubes, the pulmonary 
parenchyma, and the pleura (Fig. 88). The following classification 
of these abnormal or adventitious sounds is sufficient for clinical 
purposes : 

Rales. 

Dnf . / Sibilant. Small bronchi. 

( Sonorous. Large bronchi; trachea, 

f Crepitant. Air- vesicles; infundibula. 

Moist:- Subcrepitant. Bronchioles. 

(Mucous. Bronchi; trachea; cavities. 

Pleural Friction. Pleural surfaces. 

Splashing Sounds. 

Succussion sounds. Pleural or pulmonary cavity. 

Metallic tinkle. Pleural or pulmonary cavity. 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 65 

Extraneous sounds produced upon the surface of the body may 
prove sources of error in diagnosis, from their resemblance to 
intrathoracic adventitious sounds, such as harsh breathing, rales, 
and friction. Of these extraneous noises, perhaps the commonest 
are the so-called muscle sounds, which are comparable to a series 
of low, distant, muffled rumbles or to an interrupted humming, 
audible during both the active and the quiescent stages of breath- 
ing. Those heard during active respiration are generally attribu- 
table to the movements of the thoracic musculature or to friction 
between the patient's skin and the stethoscope; they naturally 



Moist rales. 



Dry rales. 




Mechanism of rales. 



disappear when the patient stops breathing. Those heard when 
the subject's chest is motionless are usually referable to fibrillary 
muscular contractions or to pressure upon muscular bundles by the 
chest-piece of the stethoscope; they cease when the latter is applied 
gently and evenly, and when immediate is substituted for instru- 
mental auscultation. Crackling sounds, due to the application of 
the stethoscope to a dry, hairy surface (hair crepitus), may remind 
one of crepitant rales; but these false crepitations are equally loud 
and clear with both inspiration and expiration, may be produced 
at will by the improper adjustment of the stethoscope, and disappear 



1 66 PHYSICAL DIAGNOSIS 

when the hairy part is moistened before the chest-piece is pressed 
against it. 

Rales. — In a clinical sense the term rale includes those adventi- 
tious vibratory noises due to interference with the free movements 
of the air within the bronchopulmonary structures by the presence 
of fluid or by a constriction of the bronchial lumen. According to 
the absence or the presence of liquid at their site of origin, rales are 
classed as either dry or moist; and according to their anatomic seat 
of production, as bronchial, vesicular, and cavernous; or, should they 
originate in the upper air-passages, as buccal, laryngeal, and tracheal. 

In general, it may be said of bronchopulmonary rales that they 
convey to the examiner the impression of arising deep within the lungs, 
that they are likely to be disseminated as well as circumscribed, that 
they are prone to disappear, to reappear, and to alter their situation 
as the result of deep inspiration and coughing, and that their char- 
acteristics are unaltered by external pressure over their site. Further- 
more, as Ransom has pointed out, some individuals suffering from 
bronchial catarrh whose chests are quite free from adventitious sounds 
so long as they stand upright, show abundant rales directly 
they assume the lateral decubitus. 

Dry Rales. — These are dry, snoring, whistling, or musical sounds 
of variable pitch, intensity, and quality, arising within the bronchi 
and the larger air-passages as the result of constriction of their 
lumen, due commonly to a turgescent mucosa, to spasmodic con- 
traction of the muscularis, to mechanical obstruction by masses of 
viscid, tenacious secretion, and, rarely, to extrabronchial pressure. 1 
In the tubes thus narrowed the air-columns, as they rush past the 
barrier into the wider lumen beyond, set up vibrations recognizable 
by the ear as rales, and by the hand as rhonchal fremitus (Fig. 88). 

It is convenient to classify dry rales, according to their acoustic 
properties, into two general groups — sonorous and sibilant. Sonorous 
rales are coarse, loud, low-pitched, snoring sounds arising within the 
large and the medium-sized tubes, while sibilant rales are distinguished 
by a shrill, high-pitched quality or by a soft, cooing tone, and, as a 
rule, are produced within the smaller bronchi. Exceptionally, 
however, sibilant sounds may originate within the medium-sized 
tubes, should their caliber be greatly narrowed. 

The sudden and forcible rupture, by the air-current, of delicate 
threads of mucus stretching across the bronchial lumen may account 
for the production of dry rales endowed with a peculiar snappy, 

The word rhonchus (L., rhonchus, a snoring or snorting) is frequently used 
as a synonym for the term dry rale, particularly by English writers. 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 167 

crackling quality, while the simple vibrations of similar mucous 
threads may cause rhonchi having a musical quality. The vibrations 
of a loosened bit of bronchial membrane produce a peculiar "flap- 
ping" rale of exceedingly dry quality, termed the "bruit de drapeau." 
(See Fibrinous Bronchitis, p. 180.) In interstitial emphysema coarse 
crepitations and sounds like small mucous rales have been noted, 
as the result of the action of the respiratory movements upon the 
bubbles of air imprisoned in the interalveolar walls. This so-called 
emphysematous crackling is very like the sound of the precordial 
emphysematous murmur, but the former corresponds to the respira- 
tory excursion and the latter to the heart-beats. Interalveolar 
crackling differs from intra-alveolar crepitation in being coarser, 
drier, and unrestricted to the latter part of the inspiratory cycle of 
breathing. 

Moist Rales. — These are the various moist, crackling, bubbling, 
or gurgling sounds, produced in the air-tubes and in the pulmonary 
parenchyma by the movement of air through collections of fluid 
or by the separation of agglutinated vesicular and infundibular 
walls. Such sounds, which have a distinctively moist or sticky 
quality, may be classified, according to their size, as crepitant, sub- 
crepitant, and mucous (Fig. 88). 

Crepitant Rales. — Crepitant or vesicular rales are due to the forcible 
separation of the vesicular and infundibular walls by the inspiratory 
air-columns. When these parts, glued together by a viscid or fluid 
secretion during their expiratory deflation, are forcibly separated by 
their inspiratory inflation, a series of exceedingly delicate crackling 
sounds is produced, the quality of which depends largely upon the 
density of the agglutinating material, viscid mucus affording a sticky 
sound and thin fluid a correspondingly liquid sound. The theory that 
the crepitant rale is really a form of pleural friction and not a vesicular 
sound at all, fails to carry conviction, and the weight of. opinion is 
strongly against the intrapleural origin of the sound. Owing to 
the mechanism of their production, it is obvious that crepitant rales 
occur during the latter part of inspiration, at which time full inflation 
of the vesicles occurs, with a consequent tearing apart of the adherent 
mucosa; 1 and, since all the agglutinated vesicles do not inflate simul- 
taneously, these rales are audible not as a single, isolated sound, but 
as a succession of crepitations or a shower of rales. The crepitant 

1 Very exceptionally, crepitations are audible during expiration, as in certain 
lobular infiltrations, in which, by fault of an impermeable bronchiolar obstruc- 
tion, the expiratory air-columns may be forced backward from a patch of healthy 
lung into a collection of catarrhal alveoli whose agglutinated walls are thereby 
distended with distinct crepitation. 



j 58 PHYSICAL DIAGNOSIS 

rale may be tolerably well imitated by rolling a lock of hair between 
the thumb and fingers held close to the ear, or by throwing a pinch 
of salt upon a hot stove. 

Crepitant rales are audible in croupous pneumonia during the stage 
of engorgement {crepitus indux) and during the stage of resolution 
(crepitus redux), at -which periods of the disease the pulmonary 
vesicles are partly filled with an exudate. Vesicular crepitations 
are also heard in catarrhal pneumonia, in tuberculous infiltration, 
and in the early stages of pulmonary edema, infarction, and atelecta- 
sis. Atelectatic crepitations over the bases and borders of the lungs 
are common in persons who breathe superficially, either from habit 
or from weakness, as, for example, in those of advanced age, whose 
breathing is habitually shallow, and in bed-ridden patients, whose 
alveoli are more or less deflated and unduly moist through disuse 
and posture. In such instances a brief shower of fine crepitations 
will usually be heard when the subject takes a few deep inspirations 
of sufficient force to separate the walls of the collapsed vesicles and 
infundibula; ordinarily, these atelectatic rales disappear after the 
first few deep breaths, but exceptionally they persist. 

Subcrepitant Rales, — These are moist bronchiolar sounds, audible 
during both inspiration and expiration, and due to the force expended 
by the air-columns and by the pulmonary excursions upon the con- 
tents of the ultimate bronchial tubes. Owing to the influence of these 
combined forces, deposits of viscid secretion are snapped apart and 
torn from the bronchiolar mucosa, minute bubbles of thin liquid 
are exploded, and the sticky walls of some of the finest tubes are 
alternately agglutinated and separated. The moist subcrepitations 
produced in this manner are clicking or bubbling or crackling sounds, 
which, though fine, are obviously coarser than the delicate crepita- 
tions of vesicular origin. They are not unlike the succulent sounds 
caused by agitating a mouthful of saliva with the tongue, when the 
teeth are kept in contact and the lips apart. 

Subcrepitant rales indicate the presence of pathologic secretion 
(serous, serofibrinous, purulent, or hemorrhagic) within the bron- 
chioles, and they are, therefore, to be sought for in catarrhal pneu- 
monia, in which they are referable to an exudative bronchiolitis; 
in the third stage of croupous pneumonia, when the bronchioles 
contain a liquefied alveolar exudate, and hence afford the so-called 
rale redux; and in pulmonary edema, hemorrhage, and abscess, in 
consequence of which the fine tubes are flooded with serum, biood, 
and pus, respectively. In incipient phthisis a sharp, high-pitched, 
clicking sound, known as the mucous click, is frequently audible 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 1 69 

during deep inspiration, this rale being essentially a subcrepitation 
indicative of a tuberculous catarrhal bronchiolitis. Atelectatic sub- 
crepitations, due to the inspiratory separation of partly collapsed and 
agglutinated bronchiolar walls, may occur under the conditions respon- 
sible for vesicular crepitations of this nature (q. v. s.). 

Mucous Rales. — The respiratory passage of air through accumu- 
lations of serum, pus, or blood in the larger air-passages produces 
various sized bubbling and explosive sounds, designated as mucous 
rales. Such rales ordinarily arise within the bronchi, less commonly 
within the trachea and the larynx, and, like their bronchiolar counter- 
part, the subcrepitant rale, are audible during inspiration, expiration, 
or both; their size, intensity, and pitch vary according to the diameter 
of the tube in which they originate. With air-columns of equal 
strength and with a secretion of the same density, the mucous rales 
of the primary bronchi and the upper respiratory passages are coarser, 
louder, less numerous, and lower pitched than those of the medium- 
sized bronchial twigs, between the primary tubes and the bronchioles. 
Clinically, these rales are usually defined as large, medium-sized, 
and small, according to the impression which their sound conveys 
to the mind of the auscultator. Large-sized mucous rales are well 
illustrated by the coarse, intratracheal blubbering sounds of the 
" death-rattle"; smaller types of these rales, by the more delicate 
bubblings heard in bronchitis. 

Coarse gurgling rales are produced by the passage of air through 
the fluid within a pulmonary or bronchiectatic cavity, whose bronchial 
outlet lies below the upper level of the liquid secretion that partly fills 
the excavation, the ebb and flow of air through the fluid exciting a series 
of gurgling, bubbling noises which frequently have a reverberating, 
metallic quality (Fig. 89). Similar rales may be elicited over a large 
bronchus flooded with a profuse watery secretion (Fig. 88). The 
size and the pitch of gurgling rales, whether pulmonary or bronchial, 
are largely determined by the size of the cavity in which they originate, 
the coarseness of the sound increasing and its pitch lowering, the 
larger the size of the resonating chamber. Gurgling rales are 
most clearly heard during deep, forcible inspiration, and after the 
act of coughing, in advanced phthisis, in bronchiectasis, and, rarely, 
in the exudative stage of bronchitis. 

The pulmonary fistula sound or the water-whistle noise, as it is also 
called, is demonstrable in some cases of valvular pneumothorax 
(both hydropneumothorax and pyopneumothorax) in which the 
opening of the pulmonary fistula lies below the upper level of the 
fluid within the pleural cavity. This being the case, the respiratory 



170 



PHYSICAL DIAGNOSIS 



movements of air through the liquid may set up a series of bubbling, 
gurgling rales, not infrequently endowed with a metallic, ringing 
quality. 

Cardio pneumatic rales, or moist sounds synchronous with the 
cardiac action and usually of subcrepitant or of crepitant character, 
are occasionally audible over infiltrations of the lung immediately 
adjacent to the heart. Under this circumstance rales in the bron- 
chiolar and alveolar secretion may be generated, partly by the direct 
impact of the heart and partly by the sudden variations of intra- 
thoracic pressure attending systole and diastole. 

Pleural Friction. — In health respiratory excursions of the moist, 
smooth costal and pulmonary pleurae are noiseless, but when the 




Cavernous 
gurgling 



Metallic tinkle 
Succussion sound 



Fig. 89. — Mechanism of cavernous rales and splashing sounds. 

pleural surfaces are abnormally dry and rough, as in fibrinous pleurisy 
and in tuberculosis, their movements against each other are attended 
by a sound known as pleural friction, whose quality and intensity 
vary greatly, according to the degree and extent of the lesion. (See 
Fig. 88). The friction-sound is in some instances merely a delicate 
crepitation, almost indistinguishable from a vesicular rale; in others 
it resembles a silken rustle; while in still others it sounds like a loud 
rasping rub or like the crunching of dry snow underfoot. It is more 
likely to be an interrupted than a continuous sound, and for this 
reason it may resemble, at least superficially, the jerky noise of cog- 
wheel breathing (q. v. s.) . Moreover, it is a superficial and often quite 
circumscribed sound, intensified by the pressure of the stethoscope, 
practically uninfluenced by the act of coughing, and sometimes 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 171 

accompanied by a distinct tactile fremitus. Friction is audible 
during both inspiration and expiration, but ordinarily it is most 
distinct toward the close of a deep inspiration. Although limited 
to no single area of the thorax, pleural friction is generally most 
distinct in the lower axillary region on the affected side, and jusl 
below the scapular angle (Fig. 90). Should a patch of friction dis- 
appear after having once been detected, it is frequently possible to 
demonstrate it again by Abrams' method of auscultating over the 
site of the lesion while the subject sweeps the arm of the affected side 




Fig. 90. — Common auscultatory site of pleural friction. 

upward over the head, thus moving the two pleural surfaces in a 
direction just opposite to that of ordinary respiration. 

Pleural friction is heard over the site of an acutely inflamed dry 
pleura, but it is obscured when sufficient exudate accumulates to 
lubricate and separate the inflamed membranes; with the resorption 
of the exudate, however, the sound reappears, as the frictio redux, 
which, as a rule, is louder than the primary rub. In chronic dry 
pleurisy the persistence of the friction-sound is determined by the 
chronicity and the progress of the lesion. Other factors that 
tend to destroy the normal moist and smooth state of the pleurae, 



172 



PHYSICAL DIAGNOSIS 



and hence provoke the friction-rub, are tuberculosis, neoplasms, 
and profuse diarrhea, such as that of Asiatic cholera, which inspis- 
sates the pleural cavities. It is possible that certain creaking 
sounds, virtually identical with those of genuine pleural friction, 
may arise from inflammatory changes in the intercostal muscles 
whereby intermuscular friction is excited (Coplin). The pres- 
ence of miliary tubercles beneath the pleura may be sufficient 
to produce a soft, delicate crepitation, to which Reisman has 
given the name sub pleural crepitation. Inflammation of the 
two reflected surfaces of the complementary pleura, as well as 
subphrenic peritonitis and perihepatitis, account for friction- 
rubs, not infrequently associated with tactile fremitus, over 
the lower right thorax below the sixth rib anteriorly, the eighth rib 
laterally, and the tenth rib posteriorly. (See Auscultation of the 
Abdomen.) A dry, rubbing sound over the scapula, known as 
shoulder-blade friction (Duchenne), may be due to the friction of 
this bone against the ribs, normal or necrosed; while a similar sound 
in the same situation is sometimes indicative of what Gee describes 
as shoulder-joint friction, this sound being influenced by manipula- 
tion of the subject's arm and becoming louder as the ear approaches 
the articulation. 

Perez's sign, friction sounds or crackles most intense over the 
midsternum on movement of the subject's arms at the shoulder- 
joint, may be either a dry pericardial or pleural rub generated by 
mechanical traction, or it may represent merely the transmission 
of an articular motor crackle. Ewart emphasizes the importance 
of clearly differentiating the origin of this sound by careful aus- 
cultation with a view T of localizing it to the shoulder-joint or to an 
intrathoracic area, and by noting the effects of articular move- 
ments and of respiration upon the vibrations. 

Pleuro pericardial friction is audible, most commonly toward the 
left border of the precordia, from the effect of the cardiac impact 
against the adjacent pleural surfaces, roughened by fibrinous inflam- 
matory deposits. Obviously, such sounds are synchronous with the 
movements of the heart, and it is also true that they bear a distinct 
relation to the respiratory phases. If the roughening implicates 
the pericardial and the pulmonary reflections of the pleura, the 
friction diminishes or quite disappears at the end of deep expiration, 
for during the recession of the deflated pulmonary border over the 
heart the two inflamed surfaces are not in contact (Fig. 91). If, 
on the other hand, the lesion be situated upon the pericardial and 



EXAMINATION OF THE BRONCHOPULMONARY SYSTEM 173 

the costal pleurae, the friction becomes enfeebled or lost at the end 
of forced inspiration, or when the inflated pulmonary border inter- 



Expiration. 

/fou^ened bleurae a/>cu-t. HricardlaJ. 

/Uimonary ^ — ^ —^ 



Inspiration. 
>d fileura* in contact. 




fu/monan/ 
pleura.- " 




Fig. Qi. — Mechanism of pleuropericardial friction, audible during inspiration, but 
inaudible during expiration. 

venes to separate the two roughened membranes (Fig. 92). The 
differentiation of this pleuropericardial or extrapericardial friction 

Expiration . Inspiration. 

JfoupAened Meuxae in con tad. £ os faj A^^-^. * -\f i T , ux Cos tal filet 

- ■ " - fericJrdiai pleusa. ^^Z^gg^—^icard«d pbiw-a 





Fig. 92. — Mechanism of pleuropericardial friction, audible during expiration, but 
inaudible during inspiration. 

and that of pericardial origin is described elsewhere. (See Peri- 
cardial Friction, p. 397.) 



SPLASHING SOUNDS 



Succussion Sounds. — The presence of air and fluid within a body 
cavity is determined by succussion, or the act of suddenly shaking the 
subject so as thus to create audible waves, recognized as succussion 
sounds (Fig. 89). These sounds are best appreciated by stethoscopic 
auscultation, but sometimes they are audible at some distance from the 



174 PHYSICAL DIAGNOSIS 

subject, who, indeed, may be conscious of the splashing sensation. 
Succussion sounds are highly suggestive of air and fluid within 
'the pleural cavity, their association with pneumothorax having 
been first described by Laennec — though Hippocrates was unques- 
tionably the discoverer of intrathoracic splashing (Hippocratic 
succussion sound), he misinterpreted it as a sign of empyema. 
The sounds, which generally have a hollow, metallic tone, are most 
commonly detected in hydropneumothorax, less frequently in pyo- 
pneumothorax, and exceptionally they are audible over a large 
pulmonary cavity containing fluid. Splashing sounds arising within 
the stomach and the large intestine are distinguished from those 
of intrapleural origin by an analysis of the associated physical 
signs and the localization of the sounds. Exceptionally a succus- 
sion wave can be recognized by palpation. 

Metallic Tinkling. — This sound, also termed the "falling-drop 
sound" (gutta cadens), resembles the hollow, metallic tinkling of 
drops of water falling from a height upon the surface of the fluid 
within a partly filled cistern (Fig. 89). A metallic tinkle is con- 
stantly audible in hydropneumothorax and pyopneumothorax, in 
which conditions it is provoked by deep breathing, loud speaking, 
coughing, and changes in the subject's posture. Several credible fac- 
tors have been advanced to explain this physical sign : the dropping 
of fluid from the edges of the moist, retracted lung above upon the 
surface of the pleural effusion below; the explosion of moist 
rales at the outlet of a pulmonary fistula situated above the 
level of the fluid; and the bursting of small bubbles upon the 
surface of the effusion. Metallic tinkling must be distinguished 
from the metallic consonating rales to be heard over a pulmonary 
cavity, from the reverberations of transmitted bronchial rales, and 
from the succulent sounds arising in a pneumothoracic fistula. 



SECTION IV 

DISEASES OF THE BRONCHOPULMONARY SYS- 
TEM AND MEDIASTINUM 



ACUTE CATARRHAL BRONCHITIS (Acute Tracheobronchitis; 
Acute Bronchial Catarrh) 

Clinical Pathology. — The term acute bronchitis, or tracheo- 
bronchitis, is applicable to a catarrhal inflammation, either general 
or circumscribed, affecting the mucosa of the trachea and bronchial 
tubes, but not extending to the bronchioles. Should the latter also 
be implicated (bronchiolitis) , extension to the air-vesicles (vesiculitis) 
is certain to occur, which two changes together constitute broncho- 
pneumonia. The designation of this condition as a " capillary bron- 
chitis" is unwarranted on pathologic grounds. 

The changes in the tracheobronchial mucosa consist of a primary 
hyperemia and moderate tumefaction, with degeneration and des- 
quamation of the epithelium, followed by swelling and hypersecretion 
of the mucous glands. As a rule, the exudate that bathes the inflamed 
membranes is mucous or serous, though it may have a more or less 
purulent character. According to the intensity of the process, a 
variable number of round-cells infiltrate the mucosa and submucosa, 
but, save in extremely severe cases, this process does not permeate 
far into the bronchial walls. Ordinarily, the inflammation subsides 
without complications or sequelae, and the mucosal swelling promptly 
disappears, the epithelium regenerates, the infiltrations are absorbed, 
and the secretions are removed by expectoration, leaving the mucous 
membrane of the affected parts intact and normal. Less commonly, 
the disease becomes chronic, and leads to extensive denudation and 
ulceration of the mucosa, and perhaps to permanent structural 
changes in the walls of the bronchi. 

Acute bronchitis is usually secondary to a catarrhal inflammation 
of the upper air-passages, which, by extension downward, invades the 
trachea and the bronchial tree; or, it may be symptomatic of some 
infectious disease — measles, influenza, enteric fever, malarial fever, 

175 



176 PHYSICAL DIAGNOSIS 

pertussis, phthisis, or pneumonia. The direct inhalation of irri- 
tant vapors, the insufflation of contaminated material from the 
upper respiratory tract, and the lodgment of a foreign body in an 
air-passage are additional factors of bronchial inflammation. 
Fungus tracheobronchitis, due to various identified and non- 
determined fungi, ~is frequently met with in the tropics. The 
chronic bronchitides attending gout, cardiorenal disease, asthma, 
and emphysema have from time to time ingrafted upon them acute 
exacerbations, which to all intents and purposes may be regarded as 
attacks of acute bronchitis. 

Physical Signs. — Inspection. — In simple acute bronchitis the 
information gained by inspection is more likely to be negative than 
positive. The thoracic expansion is symmetric, no anomalies of the 
respiratory movements are found, and the normal rhythm and rate 
of breathing remain undisturbed, except for a moderate polypnea, 
accompanied by a proportionate increase in the rapidity of the pulse, 
when the attack is attended by considerable fever. Actual dyspnea 
is seldom seen, save in the event of bronchiolitis and of severe sub- 
sternal pain. 

Palpation. — Vocal fremitus, as a rule, is normal, although it may 
be temporarily diminished or quite cut off over a circumscribed area 
of the lung, should the bronchus leading to such an area be plugged 
by a bit of secretion; when the obstruction is expelled by coughing, 
however, the voice vibrations immediately reappear. Rhonchal 
fremitus is palpable, especially during active inspiration, when the 
tubes contain considerable secretion. 

Percussion. — Normal pulmonary resonance is unimpaired, so long 
as the inflammation is restricted to the larger bronchi, but should 
it extend to the bronchioles and the neighboring alveoli, as it is prone 
to do in the extremes of life, patches of dulness, usually first detected 
at the bases, appear. As the result of alveolar overinflation, areas 
of moderate hyperresonance are sometimes demonstrable, particularly 
over the upper regions of the chest. 

Auscultation. — The respiratory murmur may be normal, enfeebled, 
or harsh: normal, so long as the air-currents traverse the bronchi 
without hindrance; enfeebled, if not, indeed, absent, if the lumen of 
a tube be blocked by secretion ; and harsh, often with prolongation 
of expiration, if the bronchial caliber be decidedly narrowed by a 
swollen, secretion-laden mucosa. Vocal resonance behaves like 
vocal fremitus. Bronchial rales are audible during both inspiration 
and expiration, and can usually be made to appear and disappear 
by instructing the patient to cough deeply and to breathe forcibly. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 1 77 

In the early, dry stage of bronchitis low-pitched, sonorous, and piping 
sibilant rales predominate, but later, as the liquid secretion accumu- 
lates, numerous mucous bubblings are also audible, the two types 
of adventitious sounds persisting so long as the air-tubes are narrowed 
by inflammation and rilled with secretion. 

Diagnosis. — Acute bronchitis presents a group of distinctive 
physical signs — harsh breathing and widely disseminated dry and 
moist bronchial rales, with no impairment of the normal tactile 
fremitus and pulmonary resonance. Add to these findings a history 
of having " taken cold," and of coryza, hoarseness, substernal pain, 
and cough, with little or no fever, and the diagnosis is complete. 

The possibility of mistaking pulmonary tuberculosis for simple 
bronchitis should always be thought of, since incipient phthisis may 
show little else than bronchitic signs, which, if persistent, are highly 
suggestive. In doubtful cases apical localization of such signs is 
to be sought for, the sputum stained for tubercle bacilli, and a minute 
study made of the expansion, fremitus, resonance, and breath-sounds. 

Bronchopneumonia, in affording little else than a chestful of widely 
disseminated bronchial rales, may closely resemble a simple acute 
catarrh affecting especially the smaller bronchi. But in broncho- 
pneumonia, despite the absence of tubular breathing and dulness, it 
is often possible to distinguish, amid the medley of rhonchi, the fine 
subcrepitant and crepitant rales betraying bronchiolar and alveolar 
implication, together with undue prolongation of expiration and 
unnatural hyperresonance. When these distinctive evidences of 
multiple small lobular consolidation are not apparent, the diagnosis 
must rest upon such details as urgent dyspnea, cyanosis, and 
hyperpyrexia, which are conspicuous signs of a bronchopneumonic 
process. 

Occasionally, croupous pneumonia is counterfeited by a bronchitis 
that begins abruptly with a chill, considerable fever, and blood- 
stained expectoration, and in such cases the wide-spread distribution 
and bronchitic character of the physical signs and the absence of 
evidences of lobar consolidation indicate bronchial inflammation. 

Exceptionally, the early symptoms of some infectious disease are 
temporarily masked by a coexisting bronchitis, as in certain cases 
of enteric fever, malarial fever, pertussis, and measles. In such 
instances the experienced examiner, without waiting for a complete 
clinical picture to develop, is frequently able to identify the asso- 
ciated infection by finding some one distinctive sign, such as a posi- 
tive blood-culture in typhoid, the presence of parasites in malaria, 
a mononucleosis in pertussis, and Koplik's spots in measles. 
12 



iy8 PHYSICAL DIAGNOSIS 

CHRONIC CATARRHAL BRONCHITIS (Chronic Bronchial Catarrh; 
"Winter Cough) 

Clinical Pathology. — In chronic bronchitis the bronchial mucosa 
shows a variable degree of persistent hyperemia, together with 
epithelial denudation, granular changes, and foci of ulceration. 
There is also round-cell infiltration, either implicating merely the 
mucous and submucous tissues, or extending through the entire 
bronchial wall, and perhaps leading to peribronchitis and peri- 
bronchial adenitis. In the course of time serious defects in the 
tubes tend to supervene— destruction of the mucous glands, local 
patches of atrophy and hyperplasia, areas of necrosis and ulceration, 
and bronchiectatic dilatations of various shape and size. Emphy- 
sema is a practically constant, and cirrhosis a common, associated 
pulmonary change. The retained bronchial secretion may consist 
of thin, serous fluid, glairy mucus, mucopus, or fetid purulent matter. 

Chronic bronchitis is sometimes traceable to a single attack of acute 
bronchial inflammation incident to some one of the acute infections, 
but more often it is but the relic of repeated bronchial catarrhs. 
The familiar "winter cough" of old persons means simply the annual 
lighting up of an old bronchitis that has smouldered, quiescent, 
during the warm months. In many instances, if not in most, the 
cause is primarily cardiac, renal, pulmonary, arterial, or gouty. 
Aneurism of the aortic arch is also to be recalled as a possible cause 
of intractable bronchial inflammation. 

Physical Signs. — The physical signs of chronic bronchitis are 
in no sense distinctive, for they depend not only upon the changes in 
the bronchial mucosa and wall, but also upon the character of the 
associated lesions, pulmonary, cardiovascular, or renal, as the case 
may be. In general, the findings resemble those of the acute type, 
but they are not so constant, clear cut, or well defined, and in most 
cases the coexisting emphysema and asthma conspicuously modify 
the physical signs. 

Inspection and palpation show, sooner or later, that the chest is 
overdistended, that the respiratory movements are restricted and 
labored, and that vocal fremitus is feebler than normal. Percussion, 
though frequently showing nothing abnormal, may yield a general 
hyperresonance referable to habitual overdistention of the vesicu- 
lar structure. Auscultation reveals undue expiratory prolongation, 
a confusing commingling of normal, feeble, and harsh breathing, and 
various sized dry and moist bronchial rales, indicative of different 
degrees of dry and exudative inflammation within, and spasmodic 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 1 79 

stenosis of, various parts of the bronchial tree. Should there be 
patches of collapsed lung at the bases, as is commonly the case, basal 
crepitation can be distinguished. 

Diagnosis. — Having diagnosed chronic bronchitis by the fore- 
going signs, it is important to determine whether the process be 
primary or secondary to some organic disease, and also whether 
it be associated with emphysema, asthma, bronchial dilatation, or 
other complications. 

Aside from simple chronic bronchitis, the following three special 
varieties are of clinical interest: Dry catarrh, or Laennec's catarrhe 
sec, distinguished by scanty, tenacious sputum, by severe fits of cough- 
ing, and by its common association with emphysema; bronchorrliea, 
in which there are severe paroxysms of cough, productive of aston- 
ishingly large quantities of bronchial secretion, consisting either of 
mucopurulent matter, or, less commonly, of thin, frothy, odorless 
mucus — the so-called mucous catarrh, or Laennec's catarrhe pit- 
uiteux; fetid or putrid bronchitis, characterized by disgustingly fetid 
expectoration, composed largely of pus, detritus, fatty acids, bacteria 
and various fungi, and frequently containing minute yellowish- 
brown masses — Dittrich^s or Traube's plugs. Rigors, fever, anemia, 
emaciation, and similar evidences of septic poisoning may develop 
in fetid bronchitis, and in some instances extensive damage to the 
bronchial walls, pulmonary infection, and embolic lesions of distant 
organs occur. True fetid bronchitis should not be diagnosed by 
the odor of the sputum alone, for the stench may be quite as bad 
in bronchiectasis, pulmonary abscess, gangrene, tuberculosis, and 
perforative empyema. 

FIBRINOUS BRONCHITIS (Plastic Bronchitis) 
Clinical Pathology. — This rare type of bronchial inflammation 
is distinguished by the formation, within the finer bronchial tubes, 
of fibrinous casts which become detached and are expectorated in 
the form of small gray or yellowish plugs or molds. These plugs 
can be teased out into dendritic bronchial molds, of either tubular 
or solid structure, and composed usually cf mucin, but rarely of 
fibrin. With these masses erythrocytes, leukocytes, epithelial cells, 
and Charcot-Leyden crystals are incorporated, and to their dendritic 
extremities Curschmann's spirals are commonly attached. The 
bronchial surface where the membrane forms is not conspicuously 
affected: pallor or hyperemia of the mucosa, its epithelium either 
remaining intact or being denuded, and moderate tumefaction and 
infiltration of the submucosa being the ordinary changes. 



180 PHYSICAL DIAGNOSIS 

Physical Signs. — Inspection. — Paroxysms of urgent dyspnea and 
coughing, perhaps with cyanosis and hemoptysis, are the noteworthy 
signs during the loosening and subsequent expectoration of the casts. 
Should one of the larger bronchial passages be obstructed, there may 
be inspiratory retraction of the lower intercostal spaces on the affected 
side. 

Palpation. — Ordinarily, the voice vibrations are unaltered, save 
in the event of bronchial occlusion and as the result of a complicating 
pneumonic consolidation, the fremitus being enfeebled or abolished 
in the former and exaggerated in the latter. When bronchial rales 
are plentiful, their vibrations are appreciable to the palpating hand. 

Percussion. — The percussion sound over the lungs may be resonant, 
hyperresonant, or frankly dull, according to the condition of the vesic- 
ular structure — whether normal, emphysematous, or consolidated. 
Ordinarily, however, there is more or less general exaggeration of 
the normal pulmonary resonance. 

Auscultation. — In uncomplicated cases the respiratory murmur 
is either suppressed or harsh, with a prolonged expiratory phase. 
Unnatural sharpening and intensity of the breathing should prompt 
a careful search for a patch of lobular or of lobar consolidation. 
Many moist and dry rales are audible, notably the peculiar dry 
" bruit de drapeau," due to the oscillations of bits of partly detached 
bronchial membrane. (See p. 167.) 

Diagnosis. — The physical signs of bronchitis and the expectora- 
tion of branching molds of the smaller bronchi, together point to 
fibrinous bronchitis, but, aside from these distinctive findings, it 
is well also to investigate the patient's previous history. Two 
types of the affection are recognized: a chronic recurrent form, appar- 
ently idiopathic, and characterized by paroxysms tending to recur 
periodically year after year, at approximately regular intervals; 
and an acute form, of rarer occurrence and graver outlook, which 
commonly complicates one of the febrile infections, and is distin- 
guished by dyspneic paroxysms of alarming severity, ushered in by 
a sharp attack of bronchitis, and attended by fever and rigors. 

True fibrinous bronchitis of the foregoing types is to be distin- 
guished from certain conditions sometimes attended by the accumu- 
lation of fibrin, membrane, or blood within the bronchial tubes. 
Fibrinous molds of the bronchi, for example, are occasionally expec- 
torated in pneumonia, diphtheria, phthisis, chronic cardiac disease, 
and after paracentesis of a pleural exudate. The sputum may con- 
tain blood coagula in bronchopulmonary hemorrhage, and fungus 
casts in pulmonary aspergillosis. 



DISEASES OP THE BRONCHOPULMONARY SYSTEM l8l 

BRONCHIAL ASTHMA (Spasmodic, Essential, Idiopathic, or Catar- 
rhal Asthma) 

Clinical Pathology. — The respiratory neurosis, known as bron- 
chial asthma, is distinguished clinically by recurrent, often periodic, 
paroxysms of dyspnea, cough, and viscid expectoration, accompanied 
by inspiratory thoracic rigidity and overdistention, and by depression 
and restricted mobility of the diaphragm. Spasm of the bronchial 
muscles, commonly attended by hyperemia and swelling of the mucosa 
of the smaller tubes and by a peculiar viscid bronchiolar secretion, 
chiefly explains the asthmatic attack. The bronchial spasm of itself 
is sufficient to interfere with the passage of air through the finer tubes, 
and the blocking of their lumen by a turgescent mucosa and by 
clumps of sticky mucus still further increases the difficulty. In 
addition, as Alexander Morison points out, there is also a relative, 
if not an actual, impediment to the ingress of air, and an actual 
impediment to its egress, owing to the great increase in the relative 
volume of residual intrapulmonary air existing during the asthmatic 
seizure. Repeated attacks of asthma lead to the development of 
chronic bronchial catarrh, emphysema, and dilatation of the right 
heart, and the changes incident to these complications and sequelae 
are the important pathologic findings of this neurosis. 

In a person predisposed to asthma the paroxysms may be pre- 
cipitated by an almost endless diversity of causes — by emotional dis- 
turbances, fatigue, and similar factors having a central action; 
by climatic peculiarities, irritating dust, unpleasant odors, and the 
respiratory strain of violent coughing, laughing, or sneezing, which 
probably produce bronchial stimulation; by reflex waves propagated 
from distant parts, as in the attacks excited by nasal lesions, dys- 
pepsia, and utero-ovarian disorders. Sometimes asthma supervenes 
after bronchitis, pertussis, or pneumonia, and sometimes it is directly 
related to vagus irritation depending upon mediastinal pressure. 

Physical Signs. — Inspection. — During the attack the patient's 
chest is in a state of undue inspiratory distention, the respiratory 
movements are labored, limited, and inefficient, and the excursion 
of the diaphragm is greatly restricted. Beginning as a mere oppres- 
sion in breathing, the dyspnea becomes more and more urgent until, 
as the acme of the paroxysm is reached, orthopnea supervenes, 
bringing into active play the auxiliary muscles of respiration, and 
compelling the subject to rush to an open window in his desperate 
fight for air. At this stage of the attack frequently there are cyan- 
osis, subnormal temperature, and a feeble running pulse; inspiration 



1 82 PHYSICAL DIAGNOSIS 

amounts to little more than a series of short, jerky gasps, while expir- 
ation is laboredly prolonged and wheezy, the whole picture being one 
of acute expiratory dyspnea, for deflation of the lungs is the main 
difficulty. As the acme of the attack passes, often with a violent 
fit of coughing, the breathing becomes easier, the cyanosis disappears, 
and the patient, exhausted, may fall into a deep sleep. The cough, 
until this time tight and unproductive, now loosens and the patient 
expectorates copiously, much to the relief of the respiratory distress. 
Early in the attack the sputum is scanty, and consists largely of little 
pearly beads of glairy mucus (Laennec's "perles"), which, when 
unrolled, are found to be bronchiolar casts having a peculiar spiral 
structure. These so-called Curschmanri 's spirals are composed of 
strands of mucin twisted into a tight coil in whose meshes numerous 
leukocytes (especially eosinophiles) , bronchiolar epithelium, and per- 
haps Charcot-Leyden crystals are entangled. Some of these spiral 
bodies are provided with a clear, translucent core, probably com- 
posed of a filament of transformed mucin. As the cough loosens, 
with the decline in the intensity of the paroxysm, the now abundant 
sputum becomes of a mucopurulent character, and no longer con- 
tains the Curschmann spirals. Blood-streaked sputum is common 
in severe paroxysms attended by active bronchitis. 

Other physical signs sometimes observed during an attack of 
asthma include erythema, urticaria, and angioneurotic edema of 
the upper extremities (J. S. Billings, Jr.). Very exceptionally, 
cervical emphysema is produced by the violent strain of coughing. 

Palpation. — During the paroxysm the pulmonary overdistention 
and the bronchial obstruction together enfeeble, if not abolish, vocal 
fremitus; during the interval, provided that permanent emphysema 
does not exist, the voice vibrations are normally transmitted. Pro- 
nounced rhonchal fremitus is a familiar tactile sign. The pulse 
is likely to be feeble, rapid, and intermittent or, indeed, imperceptible 
during inspiration, and the cardiac apex-beat may be effectually 
obscured by the overdilated pulmonary tissue. 

Percussion. — The percussion sound is abnormally resonant over 
both lungs, except, in some instances, at the bases, where impaired 
resonance from atelectasis may be detected. Should decided em- 
physematous distention of the lungs exist, the normal areas of 
hepatic, cardiac, and splenic flatness are correspondingly encroached 
upon. 

Auscultation. — The respiratory murmur and the cardiac sounds 
are masked by a pandemonium of rales, loud and sonorous tones 
commingled with shrill and cooing sounds, occurring early in the 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 1 83 

attack, while small and coarse mucous bubbling is audible during 
and after the acme of dyspnea. The patient, as Salter happily 
expresses it, wheezes "as if a whole orchestra of riddles were tuning 
in his chest," and oftentimes the rales are so loud that they are dis- 
tinctly heard some distance from the patient's chest; dry rales and 
mucous sounds tend to persist, after the acute seizure is past, so long 
as secretion remains within the bronchial passages. The alterations 
in vocal resonance correspond to those of vocal fremitus. 

Diagnosis. — An asthmatic paroxysm is clearly recognized by 
the physical signs, of which urgent expiratory dyspnea, hyperreson- 
ance, loud rhonchi, and viscid, pearly sputum form a distinctive 
group. These signs, plus the case-history, serve to separate asthma 
from acute bronchitis, pleurisy, phthisis, and pneumonia attended 
by excessive dyspnea, cyanosis, and restricted movements of the chest. 

Pertussis, with its sudden attacks of difficult breathing, is not 
unlike asthma, but in whooping-cough the characteristic "crow," 
the laryngeal cough, and the inspiratory type of dyspnea are dis- 
tinctive criteria. 

Certain forms of toxic dyspnea, as well as anemic shortness of breath, 
are readily differentiated from bronchial asthma, when the physical 
signs and the patient's history are studied. So-called renal, cardiac, 
and anemic "asthmas' ' are misnamed — "dyspnea' ' is the proper term 
for such disturbances, which are in no way related to true bronchial 
asthma. 

BRONCHIECTASIS (Bronchial Dilatation) 

Clinical Pathology. — Bronchiectasis is a circumscribed or a 
general dilatation of the bronchial tubes, of which two principal 
types are recognized: the cylindric, or fusiform, which affects the 
entire bronchial circumference, usually of the larger bronchi; and 
the saccular y or globular, in which the lesion consists of a pouch-like 
expansion or of a series of pockets, commonly implicating the smaller 
tubes (Fig. 93). The term bronchiolectasis is used to designate that 
uncommon condition of extensive dilatation of the bronchioles met 
with almost exclusively in the young child. Bronchiectasis univer- 
salis, also a rare form of the disease, is a congenital affection, in which 
one entire bronchial tree is converted into a series of irregular sac- 
culations. 

Bronchiectasis is most commonly situated at the pulmonary bases, 
except in the tuberculous form, which ordinarily is apical. Unilateral 
dilatation is a shade more common than bilateral, and in the former, 
implication of the right and the left bronchi occurs with about equal 



1 84 



PHYSICAL DIAGNOSIS 



frequency. In bilateral bronchiectasis the lesion is prone to be much 
more extensive in one bronchial tree than in the other. 

Acquired bronchiectasis is due primarily to weakening and lowered 
resiliency of the bronchial wall, which gives way under the stress 
of increased internal pressure or from external traction, and thereby 



Bronchial cavities 



Enlarged peribronchial 
lymph-nodes 




Bronchial cavities 



Fig. 93. — Bronchiectasis (Jefferson Hospital Laboratories). 



enlarges the bronchial lumen wherever such damage exists. Inflam- 
matory mural changes, the strain of coughing, the pressure of a large 
volume of intrabronchial secretion, and the traction exerted by peri- 
bronchial adhesions are the exciting factors essential to the formation 
of the ectases. The most important affections in which they develop 
secondarily include chronic bronchitis, tuberculosis, pleurisy, croup- 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 185 

ous and catarrhal pneumonia, influenza, pulmonary cirrhosis, ate- 
lectasis, emphysema, and bronchial obstruction from external press- 
ure by foreign bodies. 

The pathologic changes in the dilated tubes are extremely variable, 
according to the character, degree, and duration of the disease. In 
active, acute cases the mucosa has the familiar appearance of acute 
bronchial inflammation. In bronchiectases of decided chronicity, 
however, the damage is much more extensive at the seat of ectasis, 
as shown by wasting of the muscular and elastic coats, by fibrous 
thickening, and by ulceration of the mucosa. Indeed, in some 
instances little or no trace of the bronchial structure remains, the 
lesion consisting virtually of one or more irregular pulmonary cavi- 
ties, with smooth linings and thick fibrous walls — the so-called 
" trabecular bronchiectasis." Sometimes, despite extensive distri- 
bution of the lesions, there is but a scanty secretion within the 
bronchi; but Ordinarily the dilated portions are filled with 
mucopurulent material, swarming with bacteria and containing 
desquamated epithelium, and perhaps erythrocytes and bits of 
necrotic tissue, from the decomposition of which elements arises an 
intolerable fetor. Away from the seat of the dilatation the bronchi 
show, in variable degree, the changes of chronic bronchitis. In the 
neighborhood of a bronchiectatic lesion pleural adhesions and thick- 
ening commonly exist, and the lung may show patches of compression 
atelectasis, fibrosis, lobular consolidation, and emphysema. Pul- 
monary abscess and gangrene, purulent pleurisy, peritonitis, and 
cerebral abscess are other complications occasionally traceable to 
infection from the bronchiectatic secretion. Hypertrophic pulmo- 
nary osteo-arthropathy develops in certain cases of bronchiectasis, 
as the result, so Marie believes, of irritation of the osseous structures 
by toxins evolved in, and absorbed from, the bronchial lesions. 

Physical Signs. — In a considerable proportion of cases no definite 
physical signs are demonstrable, owing to the small size and deep 
situation of the lesions and to the abundance of their contained secre- 
tion. Relatively large, empty ectases near the surface (or, if deep 
seated, surrounded by consolidated lung) afford the signs of a pul- 
monary cavity, more frequently basal than apical. 

Inspection. — The subject of extensive bronchiectasis may show 
no traces of such a condition, or he may breathe laboriously, appear 
cyanotic, become emaciated, and wear the hectic facies of septic 
poisoning. The signs of Marie's disease (enlargement of the hands 
and feet with bulbous clubbing of the terminal phalanges) should 
be carefully looked for in all cases of suspected bronchial dilatation. 



!g6 PHYSICAL DIAGNOSIS 

The thorax, if at all abnormal, shows areas of deficient expansion, 
contraction, and emphysematous enlargement, with corresponding 
alterations in the respiratory excursion over these parts. The 
fluoroscope may reveal the site of the dilatation, a well-defined opacity 
being produced by an empty cavity, and a dark, circumscribed 
shadow by one filled with secretion. 

Palpation, Percussion, and Auscultation. — Over an accessible 
empty bronchiectatic cavity one expects to find increased vocal 
fremitus, a tympanitic (perhaps " cracked pot") percussion sound, 
bronchophony which may amount to clean-cut whispering pectoril- 
oquy, cavernous or amphoric breath-sounds, and moist cavernous 
rales or gurgles. With more or less constancy it is also possible 
to demonstrate the various special tonal changes of the percussion 
sound indicative of a cavity. (See p. 148.) The foregoing signs, 
however, disappear when the dilatation becomes filled with secretion 
or when the communicating bronchus becomes obstructed, but they 
reappear when the cavity is emptied and the tube cleared, as by a 
paroxysm of coughing. The tendency of the physical signs thus 
to come and go is most suggestive of a bronchiectatic cavity. Aside 
from the purely cavernous signs, those relating to coexisting bron- 
chitis, emphysema, and pleuropulmonary fibrosis are commonly 
ingrafted upon the clinical picture, and, indeed, it is not at all unusual 
for such findings to predominate. In some instances the heart is 
dislocated, by traction, toward the site of the dilatation. 

Diagnosis. — Bronchiectasis is suggested by a history of chronic 
bronchitis or of a fibroid lung or pleura in a person who tells of the 
periodic and copious expectoration of foul-smelling mucopurulent 
sputum. After standing in a conic vessel, such sputum separates 
into two strata, the lower consisting of a granular sediment of pus, 
debris, fatty acids, and hematoidin crystals, and the upper of a thin, 
mucoid liquid overlaid by dirty froth. With a history of this sort, 
the diagnosis is confirmed by the demonstration of a basal cavity 
whose special physical signs are influenced by cough, expectoration, 
and posture, but which do not alter perceptibly so as to denote pro- 
gressive increase in the size of the original excavation, even after the 
lapse of a considerable period. 

Fetid bronchitis and bronchiectasis require differentiation, since in 
both affections the patient may expectorate large quantities of evil- 
smelling, purulent material. In questionable cases the detection 
of a basal cavity is conclusive, but the presence of wide-spread bron- 
chitic signs is merely suggestive — small, deeply seated bronchiectases 
(which perhaps are part and parcel of a putrid bronchitis) defy 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 187 

recognition, at least with any degree of certainty. It is sometime 
of use to remember that in bronchiectasis there is more likelihood 
of severe constitutional symptoms and of "evacuative" cough and 
expectoration, while in fetid bronchitis the expectoration is practically 
continuous. 

Empyema with a fistulous bronchial outlet sometimes accounts for 
the sudden expectoration of a mouthful of foul, purulent matter, but 
here there are unmistakable physical signs of a pleural effusion, and 
also a helpful case-history. 

If pulmonary actinomycosis be suspected, owing to the fetor of the 
sputum, the latter should be examined microscopically for character- 
istic ray-fungus granules. The physical signs of bronchiectatic 
and pulmonary cavities are discussed under Phthisis, Pulmonary 
Abscess, and Pulmonary Gangrene. (See pp. 224, 263, and 266.) 

BRONCHOSTENOSIS (Stenosis of the Bronchi; Bronchiarctia) 

Clinical Pathology. — Narrowing or stricture of the bronchial 
lumen depends upon numerous factors relating either to obstruction 
within, or to external pressure upon, the tubes. In the former class 
of causes are included swelling of the bronchial mucosa, fibrinous 
and membranous plugs, foreign bodies, broncholiths, neoplasms, 
tuberculous lesions, and syphilitic cicatrices. To the latter group 
belong factors such as tracheobronchial adenitis, pleuropulmonary 
fibrosis, solid tumors, cysts, and abscesses of the mediastinum, 
aneurism of the thoracic aorta, large pleural and pericardial effusions, 
and extreme dilatation of the left auricle. 

According to the character of the underlying cause, bronchial 
stenoses are attended by more or less bronchitis, by local necrosis 
and ulceration, and by inflammation of the peribronchial structures. 
When a bronchus of some size is completely occluded, the pulmonary 
structure supplied by the stenotic tube is rapidly deprived of air by 
absorption, and in consequence the airless portion of the lung relaxes, 
and sooner or later collapses, this change being termed obturation 
atelectasis. In some instances the obstruction virtually serves as a 
ball-valve, allowing no air to enter the lung during inspiration, but not 
interfering with its egress during expiration. The clinical features of 
bronchial stenosis vary greatly with the character, degree, and site 
of the constriction, and, hence, with the nature of its bronchopul- 
monary sequelae, especially those affecting the distal portion of the 
lung. If a primary bronchus be obstructed, the entire lung of the 
same side is crippled; if a smaller sized tube be blocked, the circum- 



j gg PHYSICAL DIAGNOSIS 

scribed patch of the lung beyond is affected; while in bronchiolar 
stenosis, unless it be very extensive, the resulting lobular airlessness 
is usually masked by the emphysematous condition of the surrounding 
pulmonary tissue. 

Physical Signs. — On inspection there is obvious dyspnea, prin- 
cipally of the inspiratory type, ranging in intensity from moderate 
shortness of breath to extreme orthopnea with cyanosis. The respi- 
ratory movements are hurried, restricted, and inadequate, especially 
on the affected side, and they cause overaction of the auxiliary 
muscles of breathing. Inspiratory retraction of the lower ribs and 
interspaces on the side of the lesion is observed in case the residual 
air is notably exhausted and rarefied. Blocking of a large bronchus 
tends to provoke vicarious exaggeration of the thoracic movements 
on the opposite side. The foregoing signs are usually accompanied 
by paroxysmal cough, either dry and hard, or productive of sputum 
of variable amount and composition. Palpation reveals enfeebled 
or abolished vocal fremitus over the lung lying peripheral to the 
obstruction, which interferes with, or entirely damps, the trans- 
mission of the voice vibrations. Furthermore, the coexistence 
of vesicular dilatation in the neighboring pulmonary structure 
is an associated factor of diminished tactile fremitus. Percussion 
gives no noteworthy findings, save in the event of atelectasis or of 
wide-spread emphysema, which may yield, respectively, dulness 
or hyperresonance. It sometimes happens that the normal inspir- 
atory exaggeration of the percussion sound is ill defined, if not quite 
imperceptible. On auscultation loud sibilant and sonorous rales and 
numerous mucous sounds generated in the bronchial exudate are 
audible at the site of the constriction, while over the lung beyond 
the latter the respiratory murmur and vocal resonance are enfeebled 
or abolished. 

Diagnosis. — The association of inspiratory dyspnea and cough 
with circumscribed bronchial rales and a patch of airless lung indi- 
cates bronchial stenosis, the character of which is to be determined 
by finding the exciting cause of the lesion in the instance in question. 
Laryngeal obstruction, directly diagnosed by laryngoscopy, is accom- 
panied by hoarseness, urgent dyspnea, harsh, stridulous breath- 
sounds, and unnaturally extensive movements of the larynx during 
respiration. Tracheal obstruction, which does not distinctly alter 
the voice, may also provoke stridor, and is commonly attended by 
orthopnea and by limited movements of the larynx. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 189 

PULMONARY CONGESTION (Hyperemia of the Lungs) 

Clinical Pathology. — Acute or active congestion of the lungs is 
characterized by an intense engorgement of the pulmonary capillaries, 
commonly of both lungs, attended by the accumulation of blood- 
serum within the air-vesicles and by more or less swelling and shedding 
of their epithelium. A lung thus affected is larger, firmer, and less 
resilient than normal, of a dark-red color, and deficient in, though 
not wholly deprived of, air; it pits on pressure, and on section yields 




Blood-clots in 
bronchi 

Area of inflammatory 
consolidation 



Congested area 



Fig- 94 — Pulmonary congestion (Jefferson Hospital Laboratories). 

a considerable amount of bloody serum. Since acute pulmonary 
congestion commonly leads to exudative inflammation, of which it 
is, in reality, the first stage, and also tends to set up transudative 
processes, it is impossible always to recognize any clearly defined 
distinctions between these conditions. Such a condition of " active 
fluxion," typified by the stage of engorgement in an extensive croup- 
ous pneumonia, may be excited by exposure to extremes of heat 
and cold, by the inhalation of irritating vapors, by violent exercise, 



190 PHYSICAL DIAGNOSIS 

and by toxemia due to the presence of poisonous substances in the 
blood; congestion doubtless also exists in the pulmonary types of 
vicarious menstruation. Woillez's disease, or the " acute idiopathic 
pulmonary congestion" of the French school, is probably nothing 
but an abortive form of pneumonia, terminating before the stage of 
consolidation. Collateral congestion or fluxion is a form of hyper- 
emia affecting portions of the lung adjacent to some local pulmonary 
lesion, as in infarction, pneumonia, phthisis, and bronchitis. It 
arises in consequence of a local circulatory disturbance, and impli- 
cates, to a greater or less extent, the pulmonary structure not pri- 
marily diseased. 

Chronic or passive congestion of the lungs develops as the result of 
habitual stasis of the pulmonary circulation due to various conditions 
mechanically interfering with the return of blood to the heart, or 
enfeebling the cardiac force. Mechanical congestion, ultimately 
leading to a change in the pulmonary parenchyma known as brown 
induration, is a common sequel of valvular and mural disease of the 
left heart. When thus affected, the lungs are the seat of permanent 
fibrosis and pigmentation, being abnormally large, unduly firm, and 
of a dark-brown color. The connective and elastic tissues are 
increased, the capillaries are distended and tortuous, and the air- 
vesicles contain a catarrhal exudate filled with desquamated alveolar 
epithelium and leukocytes studded with pigment-granules. The 
extensive pigmentation, so characteristic of this type of chronic 
congestion, is due to hemolysis which causes erythrocytic disintegra- 
tion, some of the blood-pigment thereby liberated being ingulfed 
by the alveolar epithelium and by leukocytes and removed by expec- 
toration, while other particles are deposited, via the lymph-channels, 
in the pulmonary parenchyma. 

Hypostatic congestion, affecting the dependent parts of the lungs, 
is referable to a feeble heart plus the effect of gravity and deficient 
expansion of the pulmonary tissue. It occurs with frequency in 
various febrile and asthenic conditions that necessitate prolonged 
recumbency, and in such states it shows a special predilection for the 
bases posteriorly. It may also attend lesions of the brain, morphin- 
poisoning, and comatose states in general, and the bases of the lung 
may show this sort of congestion as a consequence of pressure exerted 
by intra-abdominal effusions and tumors. Hypostatic congestion 
is more active a process than the mechanical form, and, unlike it, 
does not set up a fibrous overgrowth. The air- vesicles are choked 
with blood-cells and the products of their destruction and with 
desquamated epithelium and serum. The congested areas are boggy 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 191 

with blood, abnormally heavy, practically airless, and dark red or 
even black-red in color, resembling, in the extreme example, the tissue 
of the spleen — hence the expression, pulmonary splenization, commonly 
applied to this change. Should edema and inflammation be ingrafted 
upon this primary engorgement, a state of hypostatic pneumonia 
is said to exist. 

Physical Signs. — Acute Congestion. — The physical signs naturally 
vary with the intensity and distribution of the process, as well as 
with the presence or absence of coexisting edema and inflammation 
in and near the congested area. If the fluxion be circumscribed, 
the evidences are much clearer, by comparison with the healthy lung, 
than if it be widely disseminated. 

Inspection ordinarily shows either a flushed face or cyanosis, dysp- 
nea, polypnea, restricted respiratory movements, cough, and perhaps 
hemoptysis, should the engorgement be very intense. On palpation, 
the vocal fremitus, if altered at all, is found to be moderately increased. 
The percussion sound is of higher pitch than normal, and the resistance 
to the pleximeter finger is somewhat exaggerated; or the defective 
resonance may still more closely approach actual dulness. Auscul- 
tation reveals either suppressed, feeble breath-sounds, or a harsh 
respiratory murmur, whose expiratory phase is comparatively high- 
pitched, prolonged, and blowing. Fine crepitant rales are audible 
when the vesicles contain serum. 

Chronic Congestion. — In chronic congestion of the mechanical 
type the most striking signs commonly relate to the underlying cardiac 
defect, which in most instances consists primarily of mitral stenosis, 
regurgitation, or both, later succeeded by right ventricular enlarge- 
ment. 

Inspection shows, apart from the cardiac findings, habitual and 
distressing dyspnea, which in time becomes true orthopnea, with 
decided cyanosis and a variable degree of anasarca. The respira- 
tory excursions, which are hurried, are notably freer at the apex 
than at the base of the lungs. There is cough, productive of con- 
siderable thin sputum, often frothy and blood-streaked, and charged 
with blood-pigment, both free and contained within alveolar epithelial 
cells — the so-called "heart-disease cells." Palpation over the bases 
gives tactile fremitus of varying grades — feeble, in a simple passive 
congestion, and increased, if much fibrosis has developed. Percus- 
sion elicits basal dulness, and above it a generally hyperresonant 
sound is frequently distinguishable. On auscultation, enfeebled, 
harsh, or even bronchial breathing is audible, according to the degree 
of congestion and attendant changes existing in the individual case; 



192 PHYSICAL DIAGNOSIS 

Simple congestion tends to obscure the breath -sounds, while dense in- 
duration of the lung intensifies them. Crepitations indicate the pres- 
ence of intravesicular fluid. In hypostatic congestion the requisite con- 
ditions usually exist to bronchialize the respiratory murmur, to impair 
resonance, and to cause mucous bubbling at the bases, but in dealing 
with this condition one also must always search for physical signs due 
to associated edema and to pneumonia. 

Diagnosis. — In detecting a pulmonary congestion the patient's 
history gives fully as important data as the physical signs, so that 
in every suspected case a thorough inquiry should be made for some 
primary factor capable of surcharging the lungs with blood, either 
by precipitating an active fluxion, or by impeding the return flow 
of blood to the left heart. This question having been decided, it 
is not difficult to interpret correctly the significance of dyspnea, 
cyanosis, cough, and frothy, bloody sputum, accompanied by basal 
signs of deficient aeration and incomplete consolidation. Conges- 
tion of the lungs versus croupous pneumonia is considered in connection 
with this infection. (See p. 217.) 



PULMONARY EDEMA (Pulmonary Dropsy; Serous Infiltration of the 
Lung; Serous Apoplexy of the Lung; Pneumochysis) 

Clinical Pathology. — In pulmonary edema the air-vesicles, their 
walls, and their communicating bronchioles are flooded with a serous 
or a serosanguinolent transudate, and in consequence of this dropsical 
condition the affected tissue becomes partly deprived of air, swollen, 
boggy, and pale. On section, the cut surface exudes a thin, frothy 
fluid, clear or tinged with blood, and containing a variable number 
of blood-corpuscles, alveolar epithelial cells, and pigment-granules. 
When edema is associated with congestion, as so often is the case, 
hyperemic discoloration is apparent, and when consolidation coexists, 
the lung is of a gelatinous consistence and appearance. The bronchi 
contain thin, frothy, blood-tinged or decidedly hemorrhagic fluid, and 
the peribronchial lymphatic glands are in some instances preter- 
naturally soft. Unless inflammatory complications are also present, 
the pleural surfaces show no noteworthy changes. Pulmonary 
edema, which may be either general or local, ordinarily implicates 
the lower lobes. Coplin, in a study of 2030 autopsies, found the 
lungs edematous in 20 per cent., the process being unilateral in 9 
per cent., and affecting the right lung a shade more frequently than 
the left. When circumscribed to the neighborhood of a pneumonic 
or other inflammatory lesion of the lung, an edema is designated as 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 1 93 

collateral, focal, or inflammatory. As the result of passive pulmonary 
hyperemia congestive edema is prone to develop in the dependent 
portions of the lungs. An acute fulminating edema of the lungs and 
bronchi is occasionally met with, especially in conditions of arterial 
and renal sclerosis, the edematous changes being attended by intense 
diffuse engorgement and by a copious outpouring of richly albuminous 
fluid containing numerous leukocytes. Vasomotor disturbances 
linked with a disproportionately forcible action of the right ventricle 
is supposed to excite this type of edema, which may rapidly cause 
death, though it sometimes recurs repeatedly in the same individual. 
The apparent determining factors of pulmonary edema are hyper- 
tension of the pulmonary circulation, plus a relative weakness of 
the leftjvenjricle, together with a hydremic blood-mass and undue 
permeability of the capillary walls. Sudden vasomotor paresis also 
is a plausible explanation in some instances. 

General edema and congestion of the lungs are frequently associated 
conditions, and have numerous factors in common — sepsis, toxemia, 
cardiac failure, exposure, and irritation of the bronchopulmonary 
mucosa. Edema is to be looked for as the terminal event in many 
illnesses, notably in nephritis, cardiac affections, grave anemias, 
cerebral diseases, acute infections, and cachectic states. It develops 
collaterally in connection with many cases of pneumonia, phthisis, 
abscess, and infarction of the lungs. Exceptionally, pulmonary 
edema is an embarrassing sequel to etherization and to thoracentesis, 
as well as a complication of angioneurotic edema of the surface of 
the body. 

Gas Edema. — The late European War furnished numerous ex- 
amples of a fulminant edema and congestion of the lungs among 
troops exposed to the irritant and toxic fumes of drift or cloud gases, 
especially those composed largely of chlorin and bromin, the former 
selectively affecting the respiratory organs and the latter the con- 
junctival surfaces. The suffocating gases (chlorin, phosgen or 
"pallite"; diphosgen, trimethylchloroforminate or "surpalite") 
cause intense irritation of the bronchioles and pulmonary alveoli 
and kill literally by a suffocative edema of the lungs. They pro- 
voke an immediate and copious outpouring of lymph throughout 
the lungs and the entire respiratory tract, and in many instances 
so extensive is this flood of liquid that a rapidly fatal asphyxia 
ensues, the subject virtually drowning in his own fluids. This 
initial asphyxial stage of gassing ordinarily is attended by a hyper- 
secretion of the salivary glands and conjunctivae and by signs of 
suprarenal inadequacy; and the subject presents a group of physical 
13 



IQ4 PHYSICAL DIAGNOSIS 

signs consisting of cyanosis, aggravated dyspnea, and hurried res- 
piratory efforts with a choking cough and free expectoration, 
primarily of thin, frothy mucus followed by a secretion of thick 
mucopurulent matter. Unlike other types of pulmonary edema, 
in which the percussion and auscultation findings are basic and 
posterior, in gas edema they relate to the upper and anterior lobes. 
Save when the clinical picture is that of collapse, the pulse is slow, 
full, and regular. 

If the patient survives the asphyxial stage, of about thirty-six 
hours' duration, there is a brief quiescence, after which a tracheo- 
bronchitic stage develops, with evidences of acute diffuse bronchitis, 
greenish-yellow sputum, hyperpyrexia, shallow polypnea, tachy- 
cardia, and delirium. If death does not occur during this stage, it 
may come later from some sequel such as pneumonia or nephritis, 
or the subject may live indefinitely, a sufferer from a chronic 
bronchitis characterized by recurring acute exacerbations. 

The foregoing dramatic clinical picture is referable primarily to 
an intense mucosal congestion of the tracheobronchial mucosa and 
to the asphyxiant effects of an exudate of thin, frothy, light yellow 
fluid of highly albuminous composition. Subsequently the terminal 
bronchi become matted together into a dense mass of congested 
material, and the lungs, of deep maroon color, are highly edematous, 
congested, and irregularly dotted with emphysematous patches and 
hemorrhagic areas. 

Physical Signs. — Inspection shows dyspnea, cyanosis, and restric- 
tion of the respiratory excursions of a degree commensurate with the 
extent of the edema and the character of its primary cause. There 
is cough, often painful, and productive of copious gushes of frothy, 
thin, serous or blood-tinged fluid. Ordinarily, unless some essen- 
tially febrile disease coexists, there are no signs of fever. Palpation 
over the water-logged, inelastic lung detects little or no vocal fremitus, 
while above it rhonchal vibrations are commonly felt. With the 
onset of an acute edema the pulse is full, bounding, and of extra- 
ordinarily high tension, but later this gives way to feebleness, arhyth- 
mia, and virtual pulselessness. Percussion yields dulness and 
increased resistance over the dropsical area, with progressive upward 
extension of the impaired resonance as the process spreads. In 
exceptional cases of fulminating edema, however, the presence of 
extensive lobular overdistention and of bronchial paralysis may 
cause general hyperresonance, despite the flooded vesicles — the so- 
called paradoxic percussion sound of Huchard. Auscultation detects 
enfeebled respiratory and voice sounds, and numerous fine moist 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 1 95 

rales over the dependent parts of the lungs. These rales, of vesicular 
and bronchiolar origin, have a distinctive liquid quality, and are 
diffused, "like a rising tide," through the lungs as the edema spreads. 
They are masked by intense, coarse, liquid bubbling sounds when 
the larger bronchi fill with the transudate. 

Diagnosis. — Having found some adequate determining cause, 
the association of basal dulness, suppressed respiratory sounds, and 
distinctively liquid rales, with labored breathing, cough, and abun- 
dant serous expectoration, is good evidence of pulmonary edema. 
A terminal edema, it should be recalled, may develop stealthily, with 
few, if any, clinical phenomena save those obtained by percussion 
and auscultation. Acute fulminating edema provokes alarming 
dyspnea and cyanosis, and is likely to arise without warning or obvious 
cause, in persons apparently in good health, the symptoms resemb- 
ling, at least superficially, pulmonary infarction, acute bronchial 
spasm, and certain inflammatory processes of the lungs and pleurae. 

Bronchial asthma, like acute pulmonary edema, is paroxysmal, 
recurrent, prone to be nocturnal, and attended by dyspnea and 
cough, but in asthma the patient usually has an accurate premonition 
of the attack, which supervenes progressively, and gives a history of 
long-standing bronchitis and emphysema, while the physical signs 
relate to a characteristic type of expiratory dyspnea, to scanty, viscid 
expectoration charged with Curschmann's spirals, to general thoracic 
hyperresonance, and to a predominance of dry bronchial rales. 

The differentiation of acute edema of the lungs from infarction, 
pneumonia, and pleurisy is detailed under these last-named subjects. 
(See pp. 197, 203, and 275.) 

PULMONARY HEMORRHAGIC INFARCTION (Pulmonary Apoplexy; 
Pnetmaorrhagia; Embolic Pneumonia) 

Clinical Pathology. — When an embolus or a thrombus plugs a 
terminal branch of the pulmonary artery and the resulting anastomo- 
sis is insufficient adequately to carry on the circulation, extravasation 
of blood takes place into the neighboring air-cells and their septa, 
thereby producing the pulmonary lesion known as hemorrhagic 
infarction. The obstructing emboli are commonly derived from 
clots lodged within the right heart, which has become dilated and 
thrombotic as a consequence of mitral obstruction, or from clots 
within one of the systemic veins; in certain instances pulmonary 
artery thrombosis has been found to be the exciting cause of an 



196 



PHYSICAL DIAGNOSIS 



infarct. The area of infarction is usually of pyramidal shape, with 
well-defined margins and base directed toward the periphery of the 
lung; such patches may be either single or multiple, and their size 
ranges from a few centimeters in the longest axis to an extravasation 
diffused through virtually an entire lobe (Fig. 95). Recent infarcts 
are dense, firm, almost airless, and of dark-red color, which in time 
changes to a dingy brown hue. Microscopically, the air-vesicles 
and bronchioles are gorged with blood-cells and the intervesicular 
walls infiltrated with the same elements. The pleura bordering 







Infarcted area 










: JS§9fl| 










m ■•■■ 






/ft 




MS" "iP 










w 

\ / 

Y 




i 



Infarcted area 
Fig- 95- — Pulmonary infarction (Jefferson Hospital Laboratories). 



upon the infarction rarely escapes plastic inflammation, and may 
exude a copious effusion into the pleural sac, while the adjacent lung 
shows a variable degree of congestion and edema, if not, indeed, 
pneumonic changes. An uncomplicated sterile infarct, after absorp- 
tion of the effused blood has occurred, generally leaves a brownish 
or slate-colored scar, though it is not impossible for the affected 
area to become entirely restored, leaving no visible trace of the infarc- 
tion. A septic infarct may be the starting-point of abscess or of 
gangrene, which latter is capable of fistulating into the pleural cavity 
and establishing a pneumothorax. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 1 97 

Physical Signs. — The physical signs of pulmonary infarction 
are substantially those of a compact local consolidation modified 
by concurrent congestion, edema, and pneumonia, and in the in- 
dividual case they vary according to the size, number, and situa- 
tion of the infarcted areas and the circulatory derangements thereby 
produced. In general, it may be stated that an infarct must have 
a peripheral extent of at least five square centimeters to afford 
definite percussion and auscultatory data, and that in central infarc- 
tions examination of the chest gives no certain information. On 
inspection there is more or less labored, painful, and hurried respira- 
tion with cough and hemoptysis, while, exceptionally, syncope and 
convulsions attend the development of an extensive infarction. If 
sterile, the latter is usually not associated with fever, but if infected, 
the familiar objective symptoms of sepsis ensue. Palpation, per- 
cussion, and auscultation afford, in typical examples, exaggerated 
vocal fremitus, dulness, bronchial breathing, bronchophony, pleural 
friction, and numerous crepitant and subcrepitant rales over a. sharply 
defined circumscribed area commonly situated posteriorly over a 
lower lobe. These signs, even though no inflammatory complications 
exist, are subject to material modifications, due chiefly to the damp- 
ing of voice vibrations by flooded bronchi, and to the masking of 
crepitations by loud rales. 

Diagnosis. — In a patient suffering from mitral disease or other 
lesion from which emboli may be derived, the abrupt onset, without 
fever, of acute respiratory embarrassment, sharp pleural pain, 
bloody expectoration, and the physical signs of a clearly delimited 
patch of pulmonary solidification are sufficient for the diagnosis. 
Infarctions due to septic emboli are recognized primarily by similar 
signs, and later by those relating to abscess or gangrene of the lung, 
as well as by the "pump-handle" temperature, recurrent rigors, 
sweats, and rapid emaciation accompanying these grave affections. 
Small deep-seated infarctions, be they single or multiple, rarely give 
rise to anything more definite than dyspnea, cough, and moderate 
hemoptysis. The distinctions between infarction of the lung and 
croupous pneumonia are given under the latter infection. (See p. 209.) 



CATARRHAL PNEUMONIA (Bronchopneumonia; Lobular, Dissemi- 
nated, or Peribronchial Pneumonia; Suffocative Catarrh) 

Clinical Pathology. — Catarrhal pneumonia is primarily an inflam- 
mation of the bronchioles and alveoli of the pulmonary lobules, 
leading to their partial or complete consolidation and to consecutive 



198 



PHYSICAL DIAGNOSIS 



hyperemia, collapse, and overdistention of the neighboring vesicular 
structures (Fig. 96). If the bronchopneumonic process be widely- 
disseminated, involving the fusion of multiple lobular lesions, an 
entire lobe may be converted into an almost airless mass of solidifica- 
tion. Almost invariably the initial lesion consists of inflammation 
of the terminal bronchioles, which rapidly invades the corresponding 
vesicles of the bronchiolar territory; in exceptional instances only 




Site of aorta 



Pneumonic infiltration 




Exudate in bronchi 



Thickened pleura 



Diaphragm 
Fig. 96.— Catarrhal pneumonia (Jefferson Hospital Laboratories). 

does the inflammation first arise within the vesicles, from primary 
disease of the septa. No special microorganism of catarrhal pneu- 
monia has been isolated, and the disease may be excited by numerous 
varieties of bacteria, such as the pneumococcus, streptococcus, 
staphylococcus, pneumobacillus, and the bacilli of influenza, diph- 
theria, leprosy, and tuberculosis, the resulting infection being far 
more frequently mixed than pure. 
The lung of catarrhal pneumonia varies considerably in gross 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 1 99 

appearance, according to the acuteness and distribution of the bron- 
chiolar and vesicular changes. Taking a well-marked acute case 
as an illustration, the organ, as a whole, is swollen, lacks resiliency, 
is unduly resistant (though not wholly deprived of air), and has a 
curiously mottled appearance, due to the presence of consolidative, 
congestive, collapsed, and overdistended areas. The bronchopneu- 
monic patches consist of red, non-crepitant, firm, nodular masses, 
surrounded by a hyperemic zone, these areas, as resolution ensues, 
turning gray and undergoing softening and absorption, with ulti- 
mate restoration of the inflamed foci. Purple spots of atelectasis, 
usually sunk below the surface of the lung, are particularly numerous 
at the base, although these evidences of lobular collapse may also 
be thickly distributed through the greater part of a lobe. Pale 
zones of emphysema impinge upon the pneumonic patches, and also 
affect the upper portions and the anterior borders of the lungs. On 
cross-section through a lobule three characteristic zones are dis- 
tinguishable, from within outward: the central distended bronchiole, 
choked with viscid mucopurulent material; a middle zone of vesic- 
ular consolidation, at first presenting a red or grayish-red, dense 
surface, which is more commonly smooth than granular, but later 
becoming paler, softer, and stippled with small purulent areas; 
and an outer zone of atelectasis, composed of collapsed, airless 
vesicular tissue, matted together by low-grade inflammation. Under 
the microscope the air-vesicles and bronchioles are found to be dis- 
tended with an exudate, wholly or almost devoid of fibrin, and rich 
in desquamated epithelium, leukocytes, and bacteria, with but few, 
if any, erythrocytes. Leukocytic infiltration of the alveolar septa 
and the walls of the terminal tubes is present to a greater or less 
degree. If resolution progresses favorably, the inflammatory pro- 
ducts soften and are disposed of by expectoration and resorption, 
and restoration of the epithelial surfaces takes place. If resolution 
be defective and infection ensues, tuberculosis, abscess, or gangrene 
may be implanted upon the vulnerable bronchopneumonic areas. 

Important concomitant pathologic changes of catarrhal pneumonia 
include pleurisy and pleural petechias, congestion and inflammation 
of the larger bronchi, and edematous swelling of the peribronchial 
glands. Empyema, meningitis, and septic arthritis are the more 
common complications, which, as a class, are rare, while exceptionally 
the cardiac muscle and the endocardium are inflamed. 

As a rule, catarrhal pneumonia arises secondarily, and this type 
of the disease is usually of streptococcal origin; primary cases ordi- 
narily are either pneumococcal or pneumostreptococcal. The dis- 



200 PHYSICAL DIAGNOSIS 

ease is most common in the extremes of life, for at these two periods 
the bronchovesicular mucosa is unusually susceptible to inflammatory 
processes and the respiratory musculature too enfeebled to insure 
thorough expulsion of the bronchiolar secretions. Catarrhal pneu- 
monia is a grave menace to life in many of the acute infections, 
notably in measles, "diphtheria, pertussis, scarlatina, variola, and 
enteric fever, and it is also prone to develop in subjects of nephritis, 
organic cardiac affections, malignant disease, rickets, emphysema, 
and other debilitating and resistance-lowering conditions. Tuber- 
culosis, syphilis, anthrax, and other specific foci in the lungs are 
attended by catarrhal inflammation of a lobular type, and the same 
is true of the several forms of pneumokoniosis. Deglutition or aspir- 
ation pneumonia, due to the insufflation of minute foreign particles, 
is met with in various comatose states (i. e., uremia and apoplexy) 
in which the sensitiveness of the upper respiratory passages is abol- 
ished. Owing to this defect, fine bits of contaminated matter (food- 
particles, for example) may be sucked into the bronchi, whose secretion 
carries the infection downward into the terminal bronchial twigs, 
and thence to the alveoli. Aspiration pneumonia is the common type 
of pneumonitis in the new-born, and it also develops as the result 
of infection from operations about the mouth and upon the upper 
air-passages, as well as in laryngeal and esophageal cancer. Ether 
pneumonia, so called, is generally of the lobular variety, and may 
prove of grave consequence in an otherwise successful operation. 
The accident doubtless arises from a number of causes — the action 
of the ether in chilling, irritating, and lowering the resistance of the 
bronchopulmonary structures, the insufflation of infectious matter 
from a contaminated inhaler, and the exposure of the patient while 
on the operating table. 

Gas pneumonia, met with in the World War, as the result of ex- 
posure to the fumes of "mustard gas" (yperite; dichlorethylsulphid) , 
occurs as a disseminated confluent lobular type, with an intense 
primary inflammation of the entire respiratory tract. The lesions 
are essentially those of wide-spread destruction of the respiratory 
mucosae consequent to the irritant action of the inhaled gas. The 
lungs, aside from areas of edema and congestion, show broncho- 
pneumonic patches which not infrequently merge so as to. implicate 
an entire lobe; the bronchi are the seat of active inflammatory 
changes, which, when purulent, tend to become predominantly 
bronchiolar and to obstruct the terminal air tubes with blood, pus, 
and masses of disintegrated shed epithelium. The foregoing con- 
dition is observed usually several hours after the subject's exposure, 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 201 

and it is attended with photophobia, lacrimation, blepharospasm, 
and cutaneous blistering, edema, and necrosis, with submucous 
gastric hemorrhages, intestinal ulceration, and renal congestion as 
troublesome later sequelae. Death generally is attributable to 
bronchiolar obstruction and to the effects of extensive coalescence 
of the bronchopneumonic consolidations ; it may occur within from 
six to sixty days after exposure to the noxious fumes (G. W. Norris). 

Physical Signs. — Inspection. — Inspection is of the utmost clinical 
value, for fulminating cases sometimes run so rapidly fatal a course 
that tactile and auditory signs fail to develop, or do so most indefi- 
nitely. Dyspnea, cyanosis, and distressing cough are the objective 
symptoms to which attention should be especially directed. The 
dyspnea, with corresponding cyanosis, is noticeable from the beginning 
of the attack, and, as the pulmonary lesion spreads, becomes progress- 
ively more acute, the patient gasping for breath with loud, jerky, 
rapid respiratory efforts, which do but little to satisfy the call for 
oxygen. In the so-called " suffocative catarrh," ending in death 
from asphyxia and cardiac paralysis, these evidences of deficient 
aeration are most strikingly exhibited. A persistent and distressing 
"grunty" cough, usually unproductive and often painful, begins 
early and lasts through the acute stages, though in fatal cases it may 
abate, despite the persistence of the other signs, a few hours before 
death. The patient's flushed cheeks and dry, hot skin are visible 
signals of the existing pyrexia. In the event of extensive basal con- 
fluence of the lobular consolidations, inspiratory drawing in of the 
lower ribs and interspaces is observed. 

Palpation. — Vocal fremitus is exaggerated if the lesions be 
sufficiently confluent and superficial to conduct the voice vibrations 
to the surface of the chest. Widely disseminated and deep infiltra- 
tions, especially if separated and surrounded by emphysematous 
areas, do not increase tactile fremitus, but, on the contrary, may 
diminish it. 

Percussion. — Early in the attack the percussion sound is unal- 
tered, and in fatal cases it may remain so until the end. But as the 
infiltrations grow and extend toward the surface of the lung, 
scattered patches of impaired resonance, sometimes amounting to 
actual dulness, can be made out. Coexisting emphysematous ter- 
ritories, however, may ingraft their quality upon the bronchopneu- 
monic sound, so that dull hyperresonance is elicited. Above the 
site of consolidation, where there is vicarious overdistention of the 
vesicles, the percussion sound is. likely to be typically hyperresonant. 

Auscultation. — The respiration is either bronchovesicular or purely 



202 PHYSICAL DIAGNOSIS 

bronchial, according to theconditionsholding in the individual case — 
broncho vesicular, if the solid patches be small and well disseminated; 
bronchial, if they crowd one another or are confluent throughout a 
considerable part of the lobe. The seat of the lesion, whether central 
or peripheral, and the condition of the adjacent vesicular structure, 
whether normal, collapsed, or distended, are active modifying influ- 
ences of the respiratory sounds. Distinct bronchophony, perhaps 
pectoriloquy, is audible over the consolidated lobules, the determining 
factors of these signs being substantially the same as those affecting 
vocal fremitus. 

Subcrepitant rales at both bases, often associated with dry and 
piping sibilant sounds, are the most typical auscultatory findings in 
catarrhal pneumonia. Finer vesicular crepitations are also detected, 
so long as the lobular solidification is not complete, and in many 
instances there are the numerous dry and moist rales of a concomitant 
bronchitis of the larger tubes. 

Diagnosis. — The gradual development of fever, rapid and labored 
breathing, cough and viscid expectoration, with subcrepitant and 
crepitant rales scattered over both bases, is highly characteristic, 
despite no distinctive modifications of the respiratory, vocal, and 
percussion sounds. Especially significant are such signs when they 
supervene in connection with one of the acute specific infections, 
or during the course of some depressing chronic affection. Distinctly 
impaired resonance, bronchial breathing, and bronchophony, though 
classic signs, can be detected only when a considerable area of con- 
solidated tissue lies within the range of auscultation and percussion, 
and in the average case of catarrhal pneumonia the diagnosis must 
rest upon the association of disseminated fine moist rales with, high 
fever and acute respiratory disturbances. In the less frequent pri- 
mary form of the infection, however, it is generally possible to map 
out circumscribed areas of consolidation which are peculiarly prone 
rapidly to clear up and to reappear in other regions. 

An ambulant form of confluent bronchopneumonia of lobar type 
in young adults is described by Riesman, who summarizes its chief 
clinical features as cough, moderate fever, and a protracted course 
characterized by absence of initial chill and critical defervescence, 
ending in complete recovery. The physical signs relate to an. 
extensive basal lobar consolidation — dulness, bronchovesicular 
respiration, and abundant showers of fine, moist crackling rales, 
frequently having a consonating quality. 

From croupous pneumonia the secondary type of catarrhal pneu- 
monia can be distinguished with ease, but the primary type only 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 203 

with difficulty, if at all. In the secondary form the gradual, insidious 
onset of the respiratory stress, the early bronchitic symptoms, the 
bilateral distribution of the chest signs, and the recovery, by lysis, 
stand in strong contrast to the abrupt onset, the predominant pleural 
symptoms, the unilateral lobar consolidation, and the critical ter- 
mination of typical croupous pneumonia. The attempt to differ- 
entiate the latter from catarrhal pneumonia of the primary type 
must needs fail in those instances in which the lobular lesions rapidly 
fuse and spread, for here the onset is abrupt, the fever high, the sputum 
rusty, and the physical signs those of dense basal consolidation. In 
this quandary the susceptibility of young children, especially under 
the age of one year, to lobular rather than to lobar inflammations, the 
fleeting tendency of a lobular pneumonia, and its likelihood of becom- 
ing definitely multiple sooner or later, are to be remembered. 

Catarrhal pneumonia versus broncho pneumonic phthisis is an impor- 
tant question to be decided, inasmuch as most of the lobular pneu- 
monias incident to measles and whooping-cough are of tuberculous 
nature. Unfortunately, in many instances the differentiation must 
be postponed until the tuberculous inroads become unmistakable, 
or until the subject comes to autopsy. A tuberculous history, great 
prostration, rapid emaciation, free sweating, recurrent hemoptysis 
tubercle bacilli and elastic tissue in the sputum, and softening, 
especially apical, are the principal hall-marks of phthisical cases. 

Acute bronchitis and catarrhal pneumonia can sometimes be dis- 
tinguished only by taking into account the relative intensity of the 
fever, cough, dyspnea, and similar disturbances in the two affections, 
for in both the physical signs may, at least for a time, be practically 
identical. (See p. 197.) 

CROUPOUS PNEUMONIA (Fibrinous or Lobar Pneumonia; Pneu- 
monitis; Lung Fever) 

Clinical Pathology. — Croupous pneumonia is an acute, self- 
limited, infectious disease, associated with a constant and character- 
istic pulmonary lesion of one or more lobes and with a distinctive 
clinical picture, due primarily to the effects of the specific pneumo- 
toxin. After a period of intense congestion the pulmonary structure 
becomes consolidated by the intra-alveolar accumulation of a coagul- 
able fibrinous exudate, which tends subsequently to undergo lique- 
faction and removal by resorption and by expectoration, thus resolv- 
ing the consolidation and restoring the original condition of the affected 
lung. Pneumonia is due to invasion of the lungs by Frankel's pneu- 



204 PHYSICAL DIAGNOSIS 

mococcus, 1 which not only evolves absorbable toxins in the local 
lesions, but itself enters the general circulation. It is still a 
moot point whether the infection arises by the inhalation of 
dried sputum charged with pneumococci or by auto-infection from 
the germs commonly resident in the healthy throat. Other bacteria 
with which the pneumococcus may be associated include Fried- 
lander's pneumobacillus, the pyogenic cocci, and the bacilli of 
enteric fever, diphtheria, and influenza. These microorganisms, 
however, probably have no direct influence in exciting true croup- 
ous pneumonia, with the exception of the first-named bacterium, 
which is regarded as the exciting factor of a grave form of pneu- 
monitis characterized by a tendency toward necrosis and suppura- 
tion — "Friedlander pneumonia." 

As a rule, pneumonia is unilateral, and implicates the greater part 
of one lobe, particularly the lower right lobe; less commonly an 
entire lung is affected, an extensive consolidation of this type being 
somewhat more frequent on the right than on the left side. The 
relative incidence of the commoner sites of primary pneumonic le- 
sions is illustrated by analysis of the statistics of 1500 cases studied 
by Ashton and Landis, by Osier, and by G. W. Norris, which shows 
that the right lung was attacked in approximately 52 per cent, of cases, 
the left lung in 35 per cent., both lungs in 14 per cent., and the apex 
of one or of both lungs in 14 per cent. In the Philadelphia General 
Hospital, about 25 per cent, of the pneumonia patients have consoli- 
dation of the right lower lobe, 22 per cent, of the left lower lobe, 12 
per cent, of the entire lung, and less than 2 per cent crossed pneu- 
monia. 

The situation of the local lesion may account for decided contrasts 
in the clinical features of different cases of pneumonia, and in con- 
sequence of this, numerous special forms of the disease have been 
exploited from time to time, usually without valid reason. Certain 
pathologic variations, however, merit separate mention, and of such 
the following seem of practical importance. Apex pneumonia, in 
which the initial consolidation invades an apex of the lung, generally 
on the right side, is met with more commonly in the child than in 
the adult, is frequently provocative of grave toxemia attended by 
striking cerebral symptoms, tends to resolve slowly, and always suggests 
the possibility of tuberculosis. Double pneumonia, implicating both 
lungs, is especially prone to affect the lower lobes, while crossed pneu- 
monia, or bilateral lesions of an opposite base and apex, more often 

1 Discovered by Sternberg, and by him named Micrococcus Pasteuri. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 205 

begins in the right upper and left lower than in the left upper and right 
lower lobes. Central or core pneumonia is the term applied to a 
pneumonic patch deep within the lung, perhaps so remote from the 
surface that no definite physical signs are afforded, or, when present, 
are not recognizable until several days after the initial chill. Should 
the pneumonitis spread in the form of a vertical slab of solidification, 
the designation stripe pneumonia is applicable. Superficial pneu- 
monia is so named because in this variety the process primarily 
affects the surface of the lung directly beneath the pleura, and hence 
the physical signs of the pneumonic lesion are peculiarly easy of 
detection and the evidences of the concurrent pleurisy conspicuous. 
(See Pleuropneumonia, p. 209.) Wandering pneumonia is a form 
of the infection that slowly and persistently creeps through the lungs, 
successively attacking lobe after lobe, either by direct continuity 
{pneumonia errans), or by the establishment of independent foci 
(pneumonia migrans) remote from the original lesion; a lung thus 
implicated may show simultaneously all stages of the pneumonic 
process, and the symptoms therefrom are likely to be protracted, 
disorderly, and grave. The adjective massive is applied to that 
form of pneumonia in which not only the alveoli, but also the bronchi, 
of a lobe, or even of an entire lung, are choked with a fibrinous exu- 
date, and in this rare condition the auscultatory physical signs are 
effectually negatived by the extensive bronchial obstruction. The 
physical signs of a massive pneumonia are very similar to those of 
pleural effusion. 

During its evolution the pneumonic lesion passes through three prin- 
cipal stages: congestion, red hepatization, and gray hepatization, 
with which it is possible to correlate more or less distinctive physical 
signs. Pathologically, these three stages are not always sharply 
defined, for a lung attacked by a rapidly spreading pneumonic inflam- 
mation may be the seat of every possible phase of the process simultan- 
eously. 

The stage of congestion or engorgement, usually lasting less than 
twenty-four hours, begins as an intense inflammatory engorgement 
of the interalveolar capillaries with the subsequent leakage of serum 
hence into the adjacent air-cells. The latter, when this stage is 
fully developed, are partly filled with a serous exudate containing a 
few leukocytes and erythrocytes, together with swollen, granular 
epithelial cells shed from the alveolar wall. Macroscopically, the 
lung appears enlarged, dark red in color, and abnormally moist; 
although denser than normal and of diminished resiliency, the pul- 



206 



PHYSICAL DIAGNOSIS 



monary tissue still crepitates, and contains sufficient air to keep it 
afloat when placed in water. 

In the stage of red hepatization or dense consolidation, of about 
four or five days' duration, the initial capillary engorgement still 




Fig. 97. — Croupous pneumonia: stage of red hepatization (Jefferson Hospital 

Laboratories). 



persists, the interalveolar walls are infiltrated and edematous, and 
the alveoli, hitherto the seat of but a moderate exudate, are now 
completely filled with a highly coagulable serofibrinous exudate, 
rich in fibrin and full of erythrocytes, leukocytes, bacteria, and 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 207 

desquamated epithelium (Fig. 97). Influenzal pneumonia com- 
monly shows disseminated necrosis of the pulmonary capillaries 
and of the epithelium lining of the alveoli, which contain a scanty 
leukocytic exudate and a thin layer of fibrin close to the walls. To 




Fig. 98. — Croupous pneumonia: stage of gray hepatization (Jefferson Hospital 

Laboratories). 

this peculiarity Le Count ascribes the tendency to hemorrhage and 
edema so commonly encountered in this type of pneumonitis, which 
essentially represents a bacteremia with localization of the toxic 
action in the blood-vessels of the lungs. 



208 PHYSICAL DIAGNOSIS 

On section, the lung appears unduly dry, although when scraped 
with a knife a small amount of sanguineous fluid mixed with 
minute fibrinous masses exudes along the track of the blade; the 
cut surface is stippled with numerous granular areas corresponding 
to the alveolar and bronchiolar coagula of fibrin. The area thus 
consolidated and enlarged is of a deep-red or brownish-red color, 
resembling a piece of liver — hence the appropriate term, red hepat- 
ization; the tissue of the lung tears easily, and is so dense and so 
airless that it neither crepitates nor floats. 

As gray hepatization and resolution supervene, the consolidation 
becomes gray or grayish-yellow in appearance, being either of a fairly 
uniform tint or mottled with patches of persistent red hepatization 
(Fig. 98) . The lung is smaller, moister, and less granular than in the 
immediately preceding stage, and, as resolution advances, the vesic- 
ular tissue becomes correspondingly crepitant; elastic, and less 
friable. These gross changes indicate subsidence of the primary 
capillary engorgement, active leukocytic infiltration of the inter- 
alveolar walls, and gradual shrinkage, softening, and liquefaction 
of the exudate. The character of the latter is now altered by the 
disappearance of the erythrocytes and of the dense fibrin network, 
and by the influx of many leukocytes which, so to speak, clean up 
much of the bacterial and cellular detritus of the vesicles by phago- 
cytosis. The exudate, having undergone fatty degeneration and 
dissolution, is finally disposed of by the lymphatics and by expectora- 
tion, complete resolution of the pneumonic area and adequate aera- 
tion of the lung being effected within a fortnight or sooner, in favor- 
able cases. Occasionally gray hepatization is succeeded by a stage oj 
purulent infiltration, in consequence of which the consolidated parts 
take on a yellowish color from their permeation by an abundant 
purulent exudate, and become soft, boggy, and exceedingly friable. 
Pus-cells flood the alveoli and extensively infiltrate the pulmonary 
connective tissue, as the result of which the lung ultimately may be 
riddled with abscesses of various size, should the process persist 
unresolved. 

Delayed resolution of the consolidation is said to exist when, despite 
the subsidence of the active pneumonic symptoms, the physical signs 
indicate the persistence of an exudate undergoing slow, imperfect 
liquefaction and removal from the alveoli. In simple delayed resolu- 
tion weeks may pass before the consolidation entirely disappears 
and the function of the lung is restored. On the other hand, the 
lung may never clear up, but, by fault of a fibroid overgrowth starting 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 209 

in the interalveolar structures, become the seat of a dense cirrhosis 
which obliterates the air-cells and greatly contracts the pulmonary 
parenchyma. In other cases pulmonary abscess is the sequel of a 
delayed resolution, and, rarely, gangrene develops. Tuberculosis 
may follow pneumonia, should the latter light up a quiescent tuber- 
culous lesion. "The instances of caseous pneumonia and softening 
which have followed an acute pneumonic process have been from the 
outset tuberculous" (Osier). 

Fibrinous pleurisy is a practically constant accompaniment of pneu- 
monia, save in deep-seated central lesions that resolve without reach- 
ing the surface of the lung. Usually the inflammation attacks the 
pleura contiguous to the pneumonic area, but it may also rapidly 
extend over the non-pneumonic lobes. Indeed, pleurisy may be 
so dominant a feature as to justify the use of the old term " pleuro- 
pneumonia." Ordinarily, the pleurisy clears up as the pneumonia 
undergoes resolution, but it may result in permanent adhesion and 
thickening of the pleural surfaces, in a richly fibrinous effusion so 
large as to require aspiration, or in an empyema removable only 
by free incision. Catarrhal bronchitis commonly is associated with 
pneumonia, and in many cases there is inflammatory enlargement of 
the bronchial glands. The larger bronchial tubes contain an abun- 
dant serous fluid with a variable amount of fibrinous material, and 
the smaller tubes traversing the pneumonic area may be choked with 
tough plugs of fibrin. Inflammation of the endocardium and peri- 
cardium are important and not very infrequent complications of 
pneumonia. Endocarditis is the commoner of the two, and more espe- 
cially implicates the valves of the left than of the right heart, particu- 
larly attacking those leaflets whose vulnerability has been heightened 
by chronic valvulitis. The pneumococcus infection may be quiescent 
and inconspicuous, or it may light up a most virulent malignant 
endocarditis, with striking toxemia, symptoms of septic embolism, 
and signs of valve destruction. Pericarditis is particularly prone 
to occur in infantile pneumonia, especially of the left lung. It may 
follow a relatively benign course, or it may result in the collection of 
a serofibrinous or purulent effusion of sufficient volume to produce 
unmistakable physical signs. Actual myocarditis, sufficiently ad- 
vanced to attract attention, rarely occurs, save as the result of pro- 
longed, intense attacks, but the heart muscle not infrequently 
shows cloudy swelling, or, rarely, more advanced degeneration. 
Arthritis is sometimes seen in association with pneumonia, especially 
in the young; the joint swelling may precede the pneumonia, appear 

during its height, or develop after defervescence. Other complica- 

14 



2IO PHYSICAL DIAGNOSIS 

tions of pneumonia of infrequent incidence include meningitis, 
neuritis, peritonitis, croupous gastritis and colitis, acute gastric 
dilatation, venous thrombosis, otitis media, and parotid bubo. 

Physical Signs. — Inspection. — The pneumonic facies is charac- 
terized by an anxious, alert expression, by flushed cheeks and shining 
eyes, by crops of herpes about the lips and nose, and by inspiratory 
gaping of the nostrils. Cyanosis is sometimes observed, but, as a 
rule, it is not conspicuous; and in the bilious type of the disease 
jaundice develops, often most intensely. The patient generally 
lies upon the affected side, and breathes rapidly, laboriously, and 
painfully, owing to the action of the pneumotoxin, to restriction of 
the aerating surface of the lungs, and to pleural pain. Very commonly 
respiration is punctuated by a peculiar and quite distinctive " expira- 
tory grunt." The dyspnea, though urgent, rarely amounts to actual 
orthopnea. The respiratory rate may be two, three, or even four times 
more rapid than normal. The typical pneumonic cough is frequent, 
dry, and painful, hence repressed. The chest movements are limited 
on the affected side, especially in extensive consolidations and in 
those accompanied by wide-spread pleurisy. On the unaffected 
side there are vicariously exaggerated respiratory movements, and 
the same thing is to be noted over the upper lobe of a lung extensively 
consolidated at its base. This condition also may mechanically 
restrict the diaphragm excursions on the side of the lesion, but in 
other instances pleural or diaphragmatic inflammation accounts for 
an absence of the normal diaphragm shadow. The cardiac impulse 
may be transmitted with undue force by dense consolidation of the 
thin wedge of the left lung which extends downward in front of the 
pericardium. 

The sputum at first is generally mucoid, but as hepatization sets 
in, exceedingly viscid, tenacious matter, often streaked with bright 
red blood, is expectorated, generally with great difficulty; later the 
sputum tends to become of red-brown hue, or "rusty." The sputum 
may be tinged yellow or green when jaundice coexists, and is thin and 
dark colored, like prune-juice, in asthenic subjects; it is abundantly 
mucopurulent when there is severe attendant bronchitis, and conspicu- 
ously hemorrhagic in severe sthenic cases; in the aged, in the very 
young, and in the debilitated little or nothing may be expectorated. 
After crisis copious puriform sputum is the rule, none at all, the ex- 
ception. Microscopically, pneumonic sputum consists chiefly of ery- 
throcytes, leukocytes, alveolar and bronchial epithelium, small 
bronchiolar casts of fibrin, and pneumococci, ordinarily mixed with 
other microorganisms. 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 211 

By x-ray examination with a fluoroscope the detection of a shadow 
toward the center or lower part of the iung is most suggestive, par- 
ticularly if, on subsequent examinations, such a shadow be found to 
change in accordance with the extension and resolution of a pneu- 
monic area. Especially in central pneumonias is the x-ray able to 
reveal consolidated patches too deep to give convincing percussion 
signs. In most instances the fluoroscope also indicates a restricted 
diaphragm excursion on the pneumonic side, and in some it shows 
cardiac displacement and even right-sided enlargement. 

Palpation. — The rapid, restricted respiratory movements and the 
unevenness of expansion noted on inspection are clearly recognized 
by the palpating palm, by which pleural friction is also occasionally 
appreciated. As the vesicles fill with the exudate, vocal fremitus 
increases, reaching its acme with complete hepatization and becoming 
normal again with the resorption of the exudate. It is important 
to remember that vocal fremitus may be entirely cut off by a coexist- 
ing pleural effusion or by the obstruction of a bronchus leading from 
the pneumonic patch. 

The pulse, full and bounding at the beginning of the attack, tends 
progressively to diminish in volume and in force as the infection 
progresses. The rate of the pulse ordinarily corresponds to the 
degree of pyrexia, but the usual pulse-respiration ratio is greatly 
disturbed, commonly ranging from 2 or 3 to 1, and, in exceptional 
cases, being practically equal. A pulse-rate exceeding 120 is a grave 
omen, save in children in whom a much greater frequency does not 
necessarily imperil life. From 150 to 170 is the usual pulse-rate 
in young children and infants affected with lobar pneumonia. 

Excessive rapidity of the pulse, irregularities of volume, and 
arhythmia are danger signals, especially "when they appear before 
crisis. 

The blood-pressure in the average case of pneumonia shows no 
noteworthy changes, but a striking hypotension is an unfavor- 
able sign. Gibson's rule is but approximate: "When the systolic 
pressure in millimeters does not fall below the pulse-rate in beats 
per minute, the fact is of good augury; when the pulse-rate per 
minute is higher than the millimeters of blood-pressure, the equi- 
librium of the circulation is seriously disturbed. " 

Percussion. — During the stage of engorgement exaggerated reso- 
nance, commonly of a Skodaic quality, is found over the affected lung, 
and a similar hyperresonance is also elicited above the level of a 
hepatized area. In pneumonia of an upper lobe Wintrich's sign 
(heightened pitch and increased intensity of the hyperresonance when 



212 PHYSICAL DIAGNOSIS 

the patient's mouth is open) is frequently demonstrable, and a cracked- 
pot percussion sound is not uncommon. As the hepatization pro- 
gresses the dulness becomes correspondingly pronounced and the 
resistance to pleximeter finger appreciably increases, but as resolution 
occurs these signs gradually disappear and sooner or later are replaced 
by normal pulmonary resonance — soon in the average case; late in 
the exceptional one, in which, despite -a typical crisis and no unfavor- 
able symptoms, the days may lengthen into weeks before the defec- 
tive resonance wholly disappears. Over a central pneumonia dulness 
develops both slowly and imperfectly, and, should such an infiltration 
resolve without invading the periphery of the lung, nothing more 
definite than a moderate impairment of resonance may be detected. 
In extensive unilateral consolidations the opposite lung is vicariously 
hyperresonant. The area of cardiac flatness may extend unduly 
beyond the right border of the sternum, and frequently the percus- 
sion limits of the liver and the spleen are enlarged. 

Auscultation. — Early during the stage of engorgement the respira- 
tory murmur ordinarily is feeble and suppressed, but as the infiltra- 
tion progresses the sound becomes harsher and more exaggerated, 
until the vesicular element is replaced first by bronchovesicular 
breathing, and later, when there is well-defined hepatization, by 
loud and tubular bronchial breathing. The latter's great intensity, 
high pitch, and distinctive "hu-u-u" quality are most conspicuous 
over a consolidation adjacent to a large, perfectly patent bronchial 
tube, and sometimes the amplication of the bronchial tone is so great 
that it is audible some distance away from the pneumonic focus. 
Usually bronchial breathing cannot be detected over a deep- 
seated central consolidation, nor is it audible if the bronchi be 
occluded, as by a fibrinous plug or by the generalized obstruction of 
a massive pneumonia. As resolution proceeds, the respiratory sounds 
lose their bronchial character, become bronchovesicular again, and 
finally acquire the breezy vesicular quality. The intensity of the 
voice resonance corresponds to that of the vocal fremitus, bron- 
chophony, and perhaps whispering pectoriloquy being heard over a 
consolidated area, and, less commonly, even egophony. 

Crepitant rales, in volleys or showers, are audible at the end of 
inspiration during the stages of engorgement and of resolution, the 
crepitus redux of the latter period being at first mingled with, 
and then replaced by, larger moist rales due to the outpouring 
of secretion into the smaller bronchi. Pneumonia in an 'emphyse- 
matous subject may afford no crepitant rales whatever, because the 
alveoli are so dilated and their walls so rigid that there can be no 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 213 

mural adhesion and separation during expiration and inspira- 
tion respectively. In young children crepitations are sometimes 
difficult to appreciate, owing to inadequate inspiratory excursions of 
the thorax. Since the vesicles and infundibula are distended by a 
fibrinous exudate during the stage of red hepatization, crepitant rales 
are then inaudible, save perhaps for an occasional isolated crackle 
produced in a vesicle which has escaped complete filling. Pleural 
friction-sounds, however, are not infrequently heard at this time, 
as well as during the other stages of the disease. Moist and dry 
rales, indicating concurrent local or general bronchitis, are Often a 
prominent associated sign, and such sounds have an extraordinarily 
sharp, resonant quality (consonating rales) when they arise within 
bronchi invested by compactly consolidated lung. 

The cardiac sounds, at first intense and clear, become distant and 
impure during the height of the fever, and relative murmurs denoting 
dilatation of the mitral and tricuspid orifices sometimes develop. 
So long as the right ventricle reacts adequately to the stress imposed 
by the intrapulmonary hypertension, the pulmonic second sound is 
accentuated and of unduly high pitch. Gradual weakening of the 
pulmonic second sound is an important sign of right ventricular 
dilatation consequent to the pulmonary engorgement, actual enfeeble- 
ment of the valvular tone being foreshadowed by a lowering of its 
vicariously heightened pitch, to which change J. M. Anders ascribes 
great value as the earliest indication of right heart failure. Irregu- 
larities of rate, rhythm, and force appear, as the strength of the 
heart flags under the influence of the fever and the pneumotoxin. 
Sudden death may occur, without warning, from acute dilatation 
or from pulmonary thrombosis. Recent studies by Porter con- 
tradict the former view that the circulatory failure in pneumonia 
is largely ascribable to vasomotor paresis. 

Diagnosis. — Frank croupous pneumonia is easily recognized, for 
in no other disease is there a more distinctive clinical picture, of 
which the facies, the painful cough and dyspnea, the rusty sputum, 
the abnormal pulse-respiration ratio, and the orderly development of 
physical signs of lobar engorgement, consolidation, and resolution 
are the noteworthy features. As a rule, these signs follow a severe 
initial chill, and are accompanied by high fever reaching its acme 
within a few hours and continuing high, with trifling fluctuations, 
for from about five to ten days, when it abruptly drops, by crisis. 
During this febrile period such laboratory findings as hyperinosis, 
leukocytosis, iodophilia, pneumococcemia, and striking deficiency 
of the urinary chlorids constitute important corroborative evidence. 



214 PHYSICAL DIAGNOSIS 

After crisis the urgent symptoms of the infection rapidly abate, 
the normal pulse-respiration ratio is reestablished, the signs of con- 
solidation clear up, and the abnormal blood and urine changes 
disappear. 

Atypical pneumonia, however, is not so well defined, and the symp- 
tomatology outlined above is subject to extraordinary modifications 
according to the ruling factors at work in the individual case, of which 
influences the most important relate to the virulence of the invading 
bacteria, the age, habits, and resistance of the patient, and the presence 
or absence of coexisting disease. Such factors as these must auto- 
matically recur to one who would deal successfully with the diagnosis 
of a disease capable of appearing in the many different guises which 
pneumonia may assume. From a clinical viewpoint, the following 
aberrant types of pneumonia are of sufficient importance to call for 
special consideration. 

Larval Pneumonia. — This is a mild, abortive, ephemeral type of 
the disease, with trifling symptoms and poorly defined physical signs, 
lasting but a few days and terminating usually by a most rapid crisis. 
In this class belongs the one-day pneumonia, which clears up by 
the second day after the onset of the initial symptoms. Many cases 
of so-called epidemic pneumonia, extensively prevailing in institutions, 
also conform to this type, though by no means is this invariably true, 
inasmuch as in certain epidemics of this sort the symptoms are severe, 
particularly those relating to the nervous and the gastro-intestinal 
systems. Epidemic pneumonia is frequently characterized by slow 
infiltration, by the rapid supervention of gray hepatization, and by a 
tendency toward connective-tissue overgrowth in the lungs. 

Toxic Pneumonia. — In contrast to the above there is a toxic or 
typhoid pneumonia, which is distinguished by grave toxic symptoms 
referable to a bacteremia, either pneumococcic or mixed. Early 
and striking prostration, serious cardiac failure, excessive diarrhea, 
tympanites, stubborn headache, delirium, and conspicuous nervous 
symptoms serve in such instances to divert attention from the real 
cause of the toxemia, which masquerades as enteric fever with severe 
initial pulmonary lesions. This typhoid pneumonia, which is merely 
pneumonia plus the "typhoid state," is to be distinguished from 
pneumotyphus , or enteric fever complicated at the outset by a croup- 
ous pneumonia which dominates the clinical picture for the first week 
or two. In typhoid pneumonia such evidences as early pneumococ- 
cemia, persistently negative Widal tests, deficient urinary chlorids, 
and absence of a roseola, together with the critical disappearance 
of both signs and symptoms, serve to rule out a concurrent Eberth 






DISEASES OE THE BRONCHOPULMONARY SYSTEM 21$ 

infection and to stamp the condition true pneumonitis with grave 
toxic manifestations. In pneumotyphus, on the other hand, the 
expected crisis fails to occur, as it should do in uncomplicated pneu- 
monia within a fortnight, and by the end of this period, at the very 
latest, the distinctive evidences of enteric fever, hitherto overshadowed 
by the pneumonia, begin to appear, as the pulmonary consolidation 
undergoes resolution and the enteric lesions approach maturity. 

Aside from these two forms of true toxic pneumonia, dulness at 
the right base posteriorly, due solely to an intense hepatic conges- 
tion and in no way related to a pulmonary consolidation, has been 
described by Lesieur and Marchand as a frequent rinding at the 
height of the disease in uncomplicated enteric fever. 

Certain cases merit the term bilious pneumonia, owing to the 
prominence of jaundice, yellowish or greenish sputum, hepatic 
engorgement, and obstinate vomiting; some of these are possibly 
true examples of toxemic jaundice, and run a severe, often fatal, 
course, while others are simply pneumonia with an associated ob- 
structive jaundice, the coexistence of which does not materially 
affect the subject's chances of recovery. 

Infantile Pneumonia. — True croupous pneumonia in infants and 
young children, though commonly attended by alarming nervous symp- 
toms, is of surprisingly low mortality. Convulsions and vomiting may 
replace the initial chill, and delirium, hyperpyrexia, abdominal pain, 
and diarrhea are conspicuous symptoms. In children old enough to ex- 
pectorate, the sputum is more likely to be scanty and mucoid, than 
profuse and rusty, in character. In about one-half of all cases of 
infantile pneumonia the patellar reflex is abolished during the stage 
of acute pyrexia; frequently the knee-jerk is lost before the develop- 
ment of the chest signs, and ordinarily it returns with crisis or 
shortly afterward. Apical pneumonia is much more common in 
children than in adults, the spread of the consolidation and its subse- 
quent resolution are less rapid, and the occurrence of pericarditis 
and of acute arthritis is more frequent. 

Senile Pneumonia. — Pneumonia in the elderly subject has an 
extremely high death-rate, and commonly begins without an initial 
chill, the onset being gradual and ill defined. The leading features 
of the attack consist of great prostration, cardiac asthenia, moderate 
fever, little or no chest pain, and slight cough, productive of scanty 
sputum, perhaps of a "prune-juice" appearance. Usually the 
physical signs, which are prone to be of a fleeting, wandering 
character, are not well marked, and, indeed, they are sometimes quite 
effectually masked by a preexisting emphysema; resolution, when it 



21 6 PHYSICAL DIAGNOSIS 

does occur, is prone to progress slowly and imperfectly, and not 
infrequently terminates in abscess or in gangrene. 

Alcoholic Pneumonia. — In the pneumonia of alcoholic sub- 
jects the symptomatology suggests delirium tremens rather than 
to pulmonary consolidation, for the clinical picture is made up 
of insomnia, incoherent muttering, and terrifying hallucinations, 
which develop insidiously, with little or no cough, fever, or chest 
pain. The expectoration is frequently like prune-juice, and may 
be quite copious. The physical signs, however, are usually char- 
acteristic, so that one cannot be excused for overlooking a pneumonic 
lung simply because the patient happens to be raving in mania a potu. 
In the majority of alcoholics pneumonia is equivalent to a death- 
warrant. 

Traumatic Pneumonia. — This term is used to designate a form of 
pneumonia secondary to violent injury of some part of the body near 
or remote from the lungs, or arising in consequence of direct laceration 
of the pulmonary tissue. The affection may occur indirectly, from 
lowered vital resistance produced by the injury, and in such instances 
the pulmonary lesion may not supervene until the subject has been 
bed-ridden for some weeks; or the pneumonia may be the direct 
consequence of a damaged lung, in which event it develops within a 
few days after the accident. Contusion pneumonia is a variety 
of pneumonitis excited by a violent blow upon the chest-wall. 

Intercurrent and Terminal Pneumonia. — In various acute specific 
infections, notably diphtheria, influenza, tuberculosis, enteric fever, 
typhus fever, bubonic plague, and malarial fever, pneumonia develops 
as a secondary, sometimes as a terminal, process. As the latter, 
it is also met with in certain chronic diseases, of which diabetes, 
arteriosclerosis, and chronic lesions of the heart and kidneys are 
typical examples. Intercurrent and terminal pneumonias are not 
uncommonly masked by the symptoms of the primary disease, and 
tend to pursue a more or less latent course, lacking the dramatic inva- 
sion, the characteristic febrile stage, and the clear-cut physical signs 
of a frank primary pneumonitis; indeed, in many instances the exist- 
ence of pneumonia is determined only after repeated and systematic 
physical examinations, and, sometimes, not until autopsy. In view 
of these facts one must, aside from the laboratory side-lights, often 
base the diagnosis upon somewhat equivocal evidence — moderate 
fever, slight increase in the pulse and respiration rates, and trifling 
cough, with impaired resonance, feeble respiration, and a few crepita- 
tions at the base of a lung. 

Aspiration and ether pneumonias, being nearly always of the lobular 
type, are dealt with under catarrhal pneumonia. (See p. 197.) 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 217 

Aside from the preceding atypical varieties of croupous pneumonia 
there remain for diagnostic consideration a group of thoracic diseases 
and certain acute infectious processes which, to a greater or less 
degree, resemble the subjective and objective symptoms of lobar 
consolidation. The first group comprises pulmonary congestion, 
edema, infarction, phthisis, catarrhal pneumonia, pleural effusion, 
and bronchitis; and to the second belong meningitis and peri- 
tonitis. 

Acute pulmonary congestion, in so far as the clinical picture is con- 
cerned, is to all intents and purposes the initial stage of croupous 
pneumonia; it is distinguished from the latter by its short duration, 
by the absence of lobar consolidation, and by the non-development, in 
orderly succession, of the attendant pneumonic phenomena. In 
this connection " one-day pneumonia" and Woillez's "idiopathic con- 
gestion" {q. v) are to be recalled. 

Hypostatic congestion usually causes dulness, harsh respiratory 
sounds, exaggerated fremitus, and crepitant rales at the bases, but 
these signs are bilateral, and, as a rule, they develop without active 
fever, rusty sputum, or herpes in a patient prostrated by some long 
illness accompanied by enfeeblement of the heart and by circulatory 
stasis in the dependent portions of the lungs. 

In acute pulmonary edema there is usually some obvious cardio- 
renal defect to explain the suddenly developing respiratory stress and 
the distinctive serous, frothy expectoration. The physical signs, in 
contrast to those of pneumonia, are bilateral, not unilobar, and tend 
rapidly to spread upward over both lungs from the bases; vocal 
fremitus and respiratory sounds are suppressed, not exaggerated; 
percussion resonance is impaired, not abolished; and the adventitious 
sounds consist of various sized liquid rales, in place of fine vesicular 
crepitations and pleural friction. Fever is absent, except in the so- 
called inflammatory edema. 

In differentiating pulmonary infarction and pneumonia the discovery 
of a source of embolism, such as mitral disease or femoral phlebitis, 
is a valuable diagnostic asset. Like pneumonia, infarction gives 
rise to sudden dyspnea, cough, pleural pain, hemoptysis, and, if the 
infarcted area be extensive, to physical signs of a dense basic infiltra- 
tion of the lung. Unlike pneumonia, infarction is attended by mode- 
rate, if any, fever, and by frankly hemorrhagic and fluid expectoration, 
while the consolidated patch is sharply circumscribed and does not 
undergo the progressive evolution of a pneumonic lesion. Evidences 
of pulmonary abscess or gangrene are to be expected when the infarc- 
tion is due to an infected embolus. 



2l8 PHYSICAL DIAGNOSIS 

Acute diffuse bronchitis, in the exceptional instance, develops most 
abruptly, with chill, fever, dyspnea, and even hemoptysis, but here 
the resemblance to pneumonia ends, for the physical signs point 
conclusively to inflammation of the tracheobronchial tree, without 
dulness or crepitations at the bases of the lungs. 

The differentiation of croupous pneumonia from catarrhal pneu- 
monia, acute pneumonic phthisis, and pleural effusion is considered 
in connection with these diseases. (See pp. 197, 222, and 275.) 

Meningitis is counterfeited by certain cases of pneumonia, especially 
by the so-called "cerebral pneumonia" of children, in whom the 
attack is ushered in by a convulsion, headache, restlessness, delirium, 
and a variable degree of cervical rigidity. Add to this group of 
symptoms herpes, leukocytosis, and arthritis, and a highly suggestive 
picture of cerebrospinal meningitis is produced. In the type of 
pneumonia under discussion, however, such a train of events means 
simply an intense meningeal congestion, and is associated with the 
signs of lobar consolidation, not uncommonly at the apex. True 
meningitis, when it complicates pneumonia, ordinarily develops at 
the height of the febrile stage, and is attended by distinctive symp- 
toms — delirium, vomiting, persistent occipital headache, irrita- 
bility, tremor, stupor, and painful retraction of the muscles of the 
neck and the back. The muscular reflexes are primarily exaggerated, 
but later abolished, and in some instances strabismus, ptosis, pupil 
changes, and various paralyses occur. Kernig's sign (inability to 
extend the leg when the thigh is flexed at right angles to the trunk) 
is of practical importance. Lumbar puncture may prove conclusive, 
the cerebrospinal fluid thus obtained showing gross changes, cyto- 
logic abnormalities, and bacteriologic findings distinctive of menin- 
geal inflammation excited by the pneumococcus, meningococcus, 
streptococcus, tubercle bacillus, or other microorganisms. (See 
page 63.) 

Peritonitis is simulated by pneumonia in which vomiting, hyper- 
pyrexia, abdominal pain, and more or less distention, tenderness, 
and rigidity of the belly-wall are conspicuous early symptoms. A 
clinical picture of this sort, which is not unusual in a child, may 
counterfeit, according to the locality of the pain, appendicitis, gastric 
ulcer, or cholecystitis, and it is safe to regard every bellyache in a 
child as a potential sign of trouble above the midriff. Irritation of 
the pleural filaments of the lower intercostal nerves is responsible 
for this variety of reflected abdominal pain, traceable to its true 
source by an analysis of the patient's clinical history and by physical 
examination of the lungs, which ordinarily reveals pneumonia of the 
lower lobe or lobes and wide-spread pleurisy. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 219 

CHRONIC INTERSTITIAL PNEUMONIA (Fibroid Pneumonia; Fi- 
broid Lang; Fibroid Induration; Pulmonary Cirrhosis or Sclerosis) 

Clinical Pathology. — Interstitial pneumonia is a chronic inflam- 
mation of the pulmonary connective tissue, attended by fibrous over- 
growth and subsequent contraction leading to permanent sclerotic 
changes in the bronchopulmonary structure (Fig. 99). According 
to the conditions prevailing in the individual case, the process origi- 
nates in the peribronchial tissues, alveoli and their walls, interlobular 



Areas of consolidation 




Area of fibrosis 



Fig. 99. — Chronic interstitial pneumonia (Jefferson Hospital Laboratories). 

septa, or pleura, ard develops subsequently into either a diffuse or 
a circumscribed fibrosis of variable extent. 

Diffuse interstitial pneumonia, commonly of unilateral distribution, 
but exceptionally implicating both lungs, not infrequently follows 
bronchopneumonia, and begins as a luxuriant peribronchial fibrosis 
spreading through the interlobular septa to the alveolar walls, and 
ultimately invading an entire lobe, or even the whole lung. More 
rarely the fibrosis is the relic of a faultily resolved croupous pneumonia, 



220 PHYSICAL DIAGNOSIS 

in which organization of the persistent intravesicular exudate and 
a fibrous overgrowth in the intervesicular septa combine to produce 
the condition termed "gray induration" at the site of the pneumonic 
infiltration. In other instances the cirrhotic changes are secondary 
to plastic inflammation of the pleura, whence fibrous bands penetrate 
the lung by way of the septa between the lobules and along the peri- 
bronchial lymphatics; or a pleural thickening and contraction may 
progressively compress the adjacent lung and set up interstitial 
changes in the atelectatic territory. Compression atelectasis, as 
by neoplasm or by aneurism, and also pulmonary syphilis are 
capable of initiating a more or less diffuse fibrosis of the lungs. 
The cirrhotic lesions arising primarily from irritation by dusts 
are considered in connection with Pneumokoniosis (p. 259), and 
the fibrosis due to tuberculosis is described under Fibroid Phthisis 
(p. 241). 

The cirrhotic areas consist of dense, pigmented collections of gray 
cicatricial tissue disseminated throughout the organ, commonly by 
peribronchial radiations between the lobules and the lobes, and ii? 
the extreme case converting, by contraction of the fibrous overgrowth, 
the lobe or even the lung into an airless, sclerotic mass of extraordi- 
narily small volume. At autopsy a lung thus damaged may be reduced 
to a compact, indurated mass of fibroid material the size of a cante- 
loupe, lying against the spinal column. In consequence of this 
unilateral shrinkage the thorax on the fibroid side is strikingly con- 
tracted and otherwise distorted (see Fig. 45), and the heart, which is 
hypertrophied, especially on the right side, is drawn toward the focus 
of the cirrhosis, along with the other mediastinal contents. The 
bronchi are generally dilated, and the air-vesicles are quite oblite- 
rated in the fibroid areas, while elsewhere both these structures 
show a variable degree of catarrhal inflammation. In the non- 
fibroid parts of the affected lung and throughout the other lung 
compensatory emphysema develops, and the pleural surfaces are 
thickened and adherent, in cases of pleurogenous origin, though 
they may escape injury in primary pulmonary fibroses. 

Aside from the foregoing lobar type, there are instances in which the 
fibrosis, though extensive, conforms more closely to a lobular dis- 
tribution, the process consisting essentially of a commingling of 
numerous indurated patches and intervening areas of emphysema. 
This variety of interstitial pneumonia, inasmuch as it is characterized 
by multiple discrete lesions situated usually at the bases and deep 
within the lungs, does not ordinarily cause the conspicuous medias- 
tinal displacement and chest deformity so distinctive of a massive, 
confluent cirrhosis. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 221 

Circumscribed interstitial pneumonia, or local fibrosis, is sharply- 
restricted to a limited area, and arises in consequence of some local 
damage to the pulmonary structure. The process is to be regarded 
as virtually reparative in character, for its tendency is to encompass 
the primary injury with an impermeable capsule of contracting con- 
nective tissue, and thus to stay the spread of infection, if not, indeed, 
to extinguish the lesion completely. Fibrous scars of this sort mark 
the sites of structural injuries of the lungs due to factors such as tuber- 
culosis, gumma, abscess, gangrene, actinomycosis, echinococcus cyst, 
and neoplastic growths. 




Fig. ioo. — Radiograph of chronic interstitial pneumonia (cf. Fig. 70). Note dense 
shadows of fibrosis through the right lung. (Plate by Dr. W. F. Manges.) 

Physical Signs. — Since the physical signs of interstitial pneumonia 
are essentially those of its clinical counterpart, fibroid phthisis, their de- 
tailed discussion will be taken up in connection with this form of tuber- 
culosis. (See p 242.) It suffices here to note that the clinical picture is 
made up of thoracic distortion and restricted respiration on the affected 
side, with enlargement and overaction of the opposite side; that the 
heart is displaced toward the site of the lesion and the anterior pul- 
monary borders may be retracted from the precordia; that over the 
cirrhotic areas increased vocal fremitus, dulness or flatness, and either 
suppressed or harsh breathing are found, while the overdistended 
territories afford hyperresonance and exaggerated breath-sounds. 



222 PHYSICAL DIAGNOSIS 

In pleurogenous fibrosis friction is to be looked for, and over areas 
of great pleural thickening, deadening of the voice and respiratory 
sounds. The cavernous signs of bronchiectasis are sometimes 
demonstrable. Accentuation and ultimate enfeeblement of the pul- 
monic second sound, with the subsequent development of the mur- 
mur of tricuspid relative insufficiency, indicates the strain upon, and 
the inevitable failure of, the right ventricle. 

Diagnosis. — Upon the foregoing signs, plus a story of cough, 
dyspnea, and mucopurulent, perhaps bloody, expectoration, per- 
sisting for many years without notably impairing the subject's strength, 
the diagnosis of chronic interstitial pneumonia is based, and the 
opinion thus formed is made still more tenable when there is a past 
history of pneumonia, pleurisy, syphilis, or local damage to the 
lung, to account for the initial cirrhotic changes. In a doubtful 
case the #-ray generally affords a certain means of diagnosis (Fig. 
ioo). The differentiation of pure pulmonary cirrhosis from so-called 
fibroid phthisis, which is not always possible when positive bac- 
teriologic findings and a clear history are wanting, is referred to 
under the latter affection. (See p. 241.) 

ACUTE PNEUMONIC PHTHISIS (Phthisis Florida? Galloping Con. 

sumption) 

Clinical Pathology. — This acute type of pulmonary tuberculosis, 
popularly known as " galloping consumption," consists of a rapidly 
spreading caseous pneumonia or bronchopneumonia, which is com- 
monly secondary to a primary apical focus of infection (Fig. 1 01). 
The vesicles and bronchioles are the seat of intense inflammatory 
changes, and are filled with an inflammatory exudate which, 
owing to its tuberculous character, does not readily undergo 
softening and expulsion, but becomes caseated; the vesicular and 
bronchiolar walls in the affected areas are infiltrated and thick- 
ened, and their blood-supply is obliterated. With the spread of the 
infection from its original site to adjacent vesicles and bronchioles, 
there is rapid implication of the entire lobule, whence the process 
spreads to adjacent lobules, either by coalescence of their lesions or 
by direct extension. The size of these patches of tuberculous con- 
solidation varies greatly in the individual case, according to the 
virulence of the infection and the resistance of the subject. In the 
so-called pneumonic type of the disease there is a diffuse, apparently 
uniform consolidation of a lobe or even of an entire lung, the changes 
closely resembling those of croupous pneumonia, both in their lobar 
distribution and, it may be, in the fibrinous character of the alveolar 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 



223 



exudate. In other cases, those of the bronchopneumonia type, the 
lesions are more widely disseminated, and conform, both in their 
lobular distribution and in the presence of a catarrhal exudate, to 
the changes produced by bronchopneumonia. In their early stages 
the tuberculous foci are recognized as white or grayish areas showing, 



Diffuse infiltration 
and softening 



Infarct. 




Cavity 
Fig. 101. — Acute pneumonic phthisis (Jefferson Hospital Laboratories). 

on microscopic examination, the histologic structure of tubercles; 
in their later stages, as caseation progresses, their color becomes 
more and more yellow; and ultimately, owing to softening, secondary 
infection and discharge of the contents of the tubercles, the lung 
may become riddled with cavities, generally of small or moderate 
size. Isolated miliary tubercles also are commonly demonstrable, 
especially toward the apices and beneath the pleura, which is generally 
thickened and covered with a fibrinous or a caseous exudate. The 
bronchi are more or less acutely inflamed, enlargement of the bron- 
chial glands is virtually constant, arid the lungs show atelectatic and 



224 PHYSICAL DIAGNOSIS 

emphysematous changes. Pyopneumothorax, from perforation of 
the pleura by a tuberculous nodule, is a complication of considerable 
frequency. 

Physical Signs. — Pneumonic Type. — The physical signs are 
essentially those of lobar consolidation, commonly of an upper lobe, 
and exceptionally of an entire lung. On inspection, it is seen that the 
patient's face bears the pneumonic flush and that the breathing is 
hurried; or there may be urgent dyspnea, with more or less bluish 
pallor and inspiratory gaping of the nostrils. The spit-cup is likely 
to contain viscid mucoid material or typically rusty sputum, in which 
tubercle bacilli may or may not be found. Palpation yields exag- 
gerated vocal fremitus over the consolidation, and sometimes reveals 
areas of restricted motility not noticed on inspection. Percussion 
shows dulness, preceding the development of which the percussion 
sound may have been decidedly hyperresonant. On auscultation 
over the affected area enfeebled breath-sounds and vesicular crepi- 
tations are heard in the early stages, succeeded by bronchovesicular 
and finally by bronchial breathing, and by intense bronchophony, 
as the consolidation progresses. These physical signs are practically 
those of ordinary croupous pneumonia, but, unlike them, they fail 
to clear up, critically, at the end of a five- or ten-day period. On the 
contrary, the consolidated areas soon begin to soften, to ulcerate, and 
to become excavated, in consequence of which cavity signs supervene 
and the sputum is charged with elastic fibers and teems with tubercle 
bacilli. This state of affairs may continue for ten or twelve weeks 
before the patient dies, but more commonly vital damage to the lungs 
is accomplished within six or eight weeks, or, in the exceptionally ful- 
minant case, within a fortnight. Occasionally the acute progress 
of the process is modified, and the disease runs its subsequent course 
as a chronic pulmonary tuberculosis, generally of the ulcerative- type. 

Broncho pneumonic Type. — This form of acute phthisis, which is 
generally bilateral, is ushered in with predominant signs of an acute 
bronchiolitis — numerous sibilant and subcrepitant rales scattered 
over both lungs. As the smaller tubes fill with cheesy material and 
the vesicles of the communicating lobules undergo catarrhal changes, 
definite evidences of the tuberculous bronchopneumonia are apparent. 
On inspection, the patient's dyspnea, cyanosis, and panting respira- 
tion attest the stress of his fight for oxygen. Palpation discovers 
scattered patches, especially apical, of increased vocal fremitus, 
over which auscultation affords bronchovesicular or even tubular 
breathing, bronchophony, and subcrepitant and crepitant rales. 
Jiirgensen's sign — the delicate crepitation of pleural tubercles — is 
sometimes demonstrable. These signs, instead of abating after two 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 225 

or three weeks, as is the rule in non-tuberculous bronchopneumonia, 
persist and are subsequently overshadowed by evidences of softening 
and excavation of the caseous foci. Sometimes the picture of the 
typhoid state supervenes, and the subject survives but three or four 
weeks; but in other instances, despite the gravity of the disease, an 
extraordinary remission occurs after the patient has been prostrated 
for several weeks, the physical signs becoming transformed into 
those of chronic phthisis with multiple cavities and considerable 
fibrosis. 

Diagnosis. — For a time croupous pneumonia may be faithfully 
counterfeited by acute phthisis of the pneumonic type, owing to its 
sudden onset, initial chill, high fever, cough, and evidences of lobar 
consolidation. At an early period there may be absolutely no means 
of differentiation, although primary implication of an apex, slow 
extension of the consolidation, and a remittent type of fever are more 
suggestive of tuberculous than of pneumococcus pneumonitis. The 
early detection of tubercle bacilli in the sputum is, of course, all 
important, but often this is not possible, and the same is apparently 
true of the ophthalmotuberculin reaction. The disease runs its 
course unchecked past the time of a pneumonic crisis without under- 
going a critical defervescence, but, on the contrary, becomes more 
and more alarming, the high fever persisting and showing greater 
fluctuations, the pulse-rate quickening, drenching sweats occurring, 
and the sputum, previously rusty or mucopurulent, becoming of 
yellowish and greenish hue and laden with tubercle bacilli and perhaps 
bits of elastic fibers. The infection now appears in its true light, 
especially as by this time the patient's emaciation and toxemia are 
pronounced and the lungs show unmistakable signs of softening over 
the areas primarily consolidated. 

In the bronchopneumonic type the differentiation from non- 
tuberculous bronchopneumonia is frequently called for, since the chief 
early symptoms are urgent dyspnea, cough, a chill or repeated rigors, 
high fever, a rapid pulse, and the physical signs of diffuse bronchioli- 
tis. In some cases, however, hemoptysis is the initial symptom, and 
it is possible to find tubercle bacilli early; but generally these are later 
signs, and one must wait for softening of the tuberculous foci, to be 
sure of the diagnosis, though the progressive emaciation of the patient 
gives no uncertain hint. A tuberculous family history and a recent 
attack of measles or of pertussis are in favor of the tuberculous char- 
acter of any obscure bronchopneumonia. 

The wide-spread bronchitis of certain cases of enteric fever may 
require discrimination, but in this disease the development of an 
15 



226 PHYSICAL DIAGNOSIS 

orderly sequence of typhoid symptoms, plus the lack of distinctive 
tuberculous physical signs, will effectually settle the question. 

CHRONIC ULCERATIVE PHTHISIS (Slow Consumption) 

Clinical Pathology. — This form of phthisis, which is primarily 
a chronic tuberculous pneumonitis, serves to illustrate every possible 
phase of damage which the lungs may suffer from invasion by the 
tubercle bacillus and by associated secondary bacterial infection. 
In the well-advanced case a most diverse group of lesions develops, 
ranging from minute miliary granules to extensive areas of destruction 
due to excavation and to fibroid overgrowth. To such a condition 
the lay term, " consumption of the lungs," is singularly applicable 
(Fig. 102). 

In the majority of cases there can be no question that the infec- 
tion is of bronchogenic origin, arising in consequence of the inhalation 
of tubercle bacilli, which lodge in the terminal bronchi or, less 
commonly, in the larger bronchial tubes. In the first instance the 
bacteria directly excite a caseous bronchopneumonia and also pene- 
trate the bronchioalveolar epithelium, thus initiating the growth 
and distribution of tuberculous foci in the surrounding connective 
tissue. These two lesions, though theoretically distinct, rapidly 
merge into a single focus, whence dissemination of the infection to 
other parts of the lungs is effected by the lymphatic vessels and by 
secondary aspiration of tuberculous material into the finer bronchial 
twigs. Exceptionally, the initial phthisical lesion is ingrafted upon 
a preexisting inflammation of the larger bronchi, which become the 
seat ot tuberculous inflammation and ulceration, whence the bron- 
chiolar and alveolar structures become secondarily infected, by aspira- 
tion. The bronchial glands are likely to be the seat of miliary and 
caseous lesions, terminating perhaps by calcification or by suppura- 
tion, often with the most disastrous results. 

Aside from its origin by inhalation, pulmonary tuberculosis may 
also arise from infection through the alimentary canal, for tubercle 
bacilli swallowed and taken into the intestines are able to penetrate, 
without exciting a local lesion, the intact mucosa of the gut, and are 
carried hence, by the lacteals and the thoracic duct, ultimately to 
lodge in the capillaries of the lungs. Children are especially sus- 
ceptible to infection along this path, which, though traveled in a 
considerable proportion of all cases of phthisis, cannot be regarded as 
the only portal of entry, to the exclusion of the older inhalation 
theory of infection via the air-passages. 

As tuberculous foci age, more and more of the lung tissue becomes 
invaded by the disease, and less and less distinction is possible between 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 



227 



the tubercles and the adjacent spots of caseous pneumonia. Exces- 
sive proliferation of connective tissue is the rule in the neighborhood 
of the tuberculous lesions, and in many such areas this reparative 
process is actually obliterative, in that it finally converts the tubercles 
into a dense cicatrix, or encapsulates them with a thick, fibrous wall, 

Small cavities 



Large cavity 







Fig. 102. — Chronic ulcerative phthisis (Jefferson Hospital Laboratories). 

which later becomes still more impermeable through calcification. 
A cheesy spot thus thoroughly inclosed or obliterated is, to all intents 
and purposes, healed, but should the fibrous envelop be too delicate, 
the infective material, even after a long period of latency, may pene- 
trate the barrier and thus light up afresh the disease. Hand in hand 
with these reparative changes the degenerative necroses of the tuber- 
cles progress, as shown by their tendency to undergo cheesy softening, 
liquefaction, and ulceration, the final result being the formation of 
cavities, many of which find a bronchial outlet by ulcerative extension. 
The wall of such a cavity is formed of a fibrous overgrowth lined by 
a pyogenic membrane, and its contents consist of foul mucopurulent 
secretion swarming with both pyogenic and tubercle microorganisms 



228 PHYSICAL DIAGNOSIS 

and laden with caseous masses, elastic tissue, degenerate epithelium, 
and blood- and pus-cells. A cavity may enlarge by the process of 
chronic ulcerative erosion kept up by the combined action of pyogenic 
cocci and tubercle bacilli; and several moderate-sized cavities may 
fuse into a single large excavation, or they may form a chain 
of communicating chambers. Some cavities are but one or two 
centimeters in diameter, while others destroy practically an entire 
lung. A blood-vessel-that has escaped thrombotic obliteration within 
a cavity is to be regarded as a possible source of serious, even fatal, 
hemorrhage, the blood issuing either from a breach eroded in the 
vessel-wall, or from the rupture of an aneurismal dilatation of a 
vessel (Rasmus sen's aneurism) in the lining membrane of the cavity 
or bridging it from wall to wall. It is obvious that in a cavity with no 
bronchial outlet such a hemorrhage is not betrayed by hemoptysis, 
this accident being a so-called " concealed hemorrhage" of phthisis. 
Aside from the foregoing types of cavity, there are those of bronchiec- 
tatic origin, due to the dilatation of small bronchi weakened by 
tuberculous ulceration and distended by accumulations of secretion 
pent up within the diseased tubes. These have been referred to 
in the discussion of bronchiectasis. (See Fig. 93). 

The pleura in a case of chronic ulcerative phthisis rarely, if ever, 
escapes injury, either in the form of a simple dry pleurisy with adhe- 
sion and thickening, or as a tuberculous invasion by miliary and 
caseous foci. Pleural effusions and pyopneumothorax are likewise 
to be reckoned with in numerous instances. The non-tuberculous 
pulmonary tissue is generally overdistended in its endeavor vicariously 
to offset the crippling effects of the phthisis, and in many areas 
atelectasis and compression of the lung are apparent. 

About 1 per cent, of all cases of pulmonary tuberculosis is 
attended by chronic valvular disease of the heart, which only ex- 
ceptionally is of tuberculous nature, and the latter is true also of 
pericarditis, a rare complication usually arising secondarily by ex- 
tension from the pleura or from a cavity. Tuberculosis of the heart 
muscle is exceptional, but myocardial degeneration is common. 
The size of the heart is commonly smaller than normal in phthisical 
subjects, and this change is variously attributed to factors such as 
congenital anomalies, general cardiovascular hypoplasia, and the 
effects of habitual inspiratory restriction. Right-sided dilatation 
occurs as the result of long-standing pulmonary fibrosis and asso- 
ciated changes which strain the right ventricle ; and in such cases 
loss of compensation and the onset of cardiac failure hastens the 
progress of the pulmonary infection. 

Mitral regurgitation is by far the commonest valvular defect in 









DISEASES OF THE BRONCHOPULMONARY SYSTEM 229 

phthisical patients. It has little or no effect upon the pulmonary 
lesion, although if compensation be good it may retard its progress 
(Lawrason Brown). Pulmonary stenosis, in that it causes per- 
sistent pulmonary anemia, predisposes to phthisis ; while the effect 
of mitral stenosis, which sets up a constant congestion of the 
lungs and concentrates in them the immunizing agents of the 
blood, is supposed to be more or less antagonistic. Aortic disease 
is more commonly associated with latent than with active types 
of pulmonary tuberculosis. 

In incipient phthisis lowered blood-pressure with acceleration of 
the pulse-rate is the rule, and as the disease advances both signs 
grow more conspicuous, owing to degeneration of the myocardium 
from the effect of the tuberculous virus. 

Aside from the secondary infections that may attack various 
parts of the respiratory tract, the important complications of 
phthisis include tuberculosis of the intestines, kidneys, lymphatic 
glands, meninges, and ischiorectal abscess. 

Usually the initial lesion of chronic ulcerative phthisis develops 
in the upper lobe of one lung (most commonly the right) at a point 
one or one and one-half inches (2.5 to 3.75 cm.) below its extreme 
apex (Kingston Fowler) , whence the process tends to spread down- 
ward on the same side, and later to the apex of the opposite lung, 
as the result of which method of extension the apical lesions are likely 
to be older and more advanced than those of the bases. Exception- 
ally, the starting-point of the disease is in a lower lobe, such instances 
occurring more commonly in children than in adults. In the con- 
dition termed "hilus tuberculosis," primarily affecting the roots of 
the lungs and thence spreading toward the surface, extensive de- 
struction of both lungs may afford atypical and equivocal signs for 
a protracted period. (See p. 240.) Clinically, the earliest phys- 
ical evidences of phthisis usually are demonstrable either an- 
teriorly, just below the center of the clavicle and below the outer 
third of this bone in the first and second interspaces, or posteriorly 
in the supraspinous fossa. Infection of the lower lobe begins poster- 
iorly at a point about i§ inches (3.75 cm.) below its summit (Kingsley), 
the physical signs of such an invasion being found at a spot opposite 
the fifth thoracic vertebra, whence they spread downward and out- 
ward along the line of the vertebral border of the scapula, when it 
is elevated by having the subject place the hand upon the opposite 
shoulder with the elbow raised above this level. 

Although no case of phthisis can be expected to run a clinical 
course, divisible into fixed, well-defined stages, it seems best, when 
examining a suspected case of this disease, to have in mind certain 



23° 



PHYSICAL DIAGNOSIS 



arbitrary periods of the infection, so as intelligently to correlate the 
physical signs with the underlying pulmonary lesions. It is, therefore, 
convenient to divide the disease into three periods, 'which, it is per- 
fectly obvious, must overlap, merge, and variously dominate the 
clinical picture, according to the peculiarities of the process in the 
individual patient. The first period, which includes the stage of 
initial tuberculous deposits, may exist for some time and yet afford 
no definite physical signs; and in this category belong the so-called 
" incipient" cases, with suspicious histories and negative or trifling 
signs, as well as those with clear evidences of one or more circum- 
scribed, limited areas of infiltration. The second period, correspond- 
ing to the wider dissemination and softening of the infiltrations, 
comprises cases with single or multiple lesions undergoing degener- 
ative changes, the objective symptoms of which are conspicuous. 
The third period, that of cavity formation, affords signs of pulmonary 
excavation and extensive fibrosis, with extension of the infiltration 
and softening originally determined. 

Physical Signs. — Inspection. — In incipient cases one must often 
be content to gain information from minor stigmata rather than from 
characteristic hall-marks of the disease. Typical illustrations of 
such stigmata have been perpetuated in Botticelli's pallid angels, 
and in Rosetti's and Burne- Jones's lanky beauties, whose wistful, 
pained faces, long, slender necks, and stooped, flat-chested trunks 
are highly suggestive of early phthisis. As Iwai has shown, super- 
numerary breasts are twice as common in phthisical as in healthy 
women. The characteristics of the phthisical or alar type of thorax 
will be found in a foregoing section. (See p. 80.) In this con- 
nection it is interesting to note that Rothschild' 's sign (preternatural 
flattening and mobility of the sternal angle) is frequently demon- 
strable long before the first signs of infiltration appear. Ankylotic 
rigidity of the spinal column, especially of the thoracic and lumbar 
segments {Lorenz's sign), also is found in a considerable percentage 
of patients with incipient phthisis. 

Progressive loss of weight is a prominent early finding, which, as 
the disease advances, becomes correspondingly more conspicuous, 
the emaciation sometimes attaining a most extraordinary degree. 
(See Fig. 25, p. 81.) In some persons phthisis may be active for a pro- 
longed period without apparently making inroads upon the general 
health and nutrition. A striking phase of the present European 
war is the physical fitness and ability for stress shown by the large 
number of tuberculous soldiers among the armies engaged. Guil- 
haud even goes so far as to describe a form of phthisis characterized 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 23 1 

by obesity, regarding it as readily curable and not incompatible 
with longevity. 

The trained eye appreciates the pertinence of the tuberculous 
fades; an oval face, with delicate or pinched features; bright, ap- 
pealing eyes, with dilated, perhaps unequal, pupils and snow-white 
scleras; and, as the disease progresses, respiratory dilatation of 
the nasal alae and bright-red hectic flushes upon either cheek 
(Fig. 103). Gee's trenchant remark, "we should never see anemia 
without thinking of phthisis," should serve as a maxim for daily 
use in dealing with chest cases, although blood deterioration 
ordinarily does not occur until malnutrition and sepsis have long 
been at work. 




Fig. 103. — The phthisical fades (Jefferson Hospital). 

Incipient apical disease is early betrayed by deficient expansion 
and flattening of one infraclavicular space, the former defect 
usually being more easily recognized by palpation than by in- 
spection (v. i.). Lagging or complete respiratory immobility of 
the acromion process on the affected side is another early sign of 
real value. Diminished pulmonary elasticity plus spasmodic mus- 
cular contraction accounts for these early physical signs, and if 
persistent the combined factors lead to actual degeneration of the 
muscles affected, according to Pottenger's studies. The trapezius 
and the sternocleidomastoid muscles are notably smaller, softer, 
and shorter on the affected side in unilateral apical lesions. 

As softening and fibrosis increase the neck apparently lengthens, 
the supraclavicular and infraclavicular regions deepen conspicu- 
ously, and the clavicles become abnormally prominent; the inter- 
spaces sink in, the ribs overlap, the scapula on the affected side 



232 PHYSICAL DIAGNOSIS 

tilts outward, and circumscribed areas of immobility, flattening, 
and retraction appear upon the chest-wall, the expansion of which 
progressively diminishes as the result of the pulmonary destruc- 
tion and the pleural pain. These changes, consisting essentially 
of reflex muscle spasm and atrophy, are largely attributable to 
disorders of the thoracic sympathetic ganglion and to irritation 
of the vagus, the brachial plexus, and the phrenic and intercostal 
nerves (Pomeroy; Balint; Jessen). In extensive unilateral lesions 
the opposite half of the thorax may be vicariously overdis tended. 

More or less restriction of Litten's diaphragm shadow on the 
affected half of the thorax may be evident, generally in consequence 
of pleural pain; and reversal of the physiologic respiratory type is 
a common anomaly of breathing in incipient tuberculous deposits. 

A diffuse cardiac impulse, visible in the second, third, and fourth 
left interspaces, is commonly found in advanced tuberculosis of the 
left apex, in consequence of fibrous retraction of the lappet of lung 
from its normal site between the heart and the thoracic wall. 
Displacement of the apex to either side (more frequently to the 
left) occurs very frequently, as the result of either traction or 
pressure. 

Not infrequently a delicate tracery of small venules courses over 
the lower part of the anterior chest-wall, and many phthisical sub- 
jects are disfigured by a downy growth of hair, by dirty brownish 
patches of tinea versicolor, especially upon the back, and by chloasmic 
discoloration {chloasma phthisicorum) of the face. In tubercular 
children with a tuberculous family history Gibson has noted the 
frequent occurrence of numerous visible venules upon the chest and 
face, associated with undue prominence of one or both jugulars, 
the vessels thus overdistended failing to show a normal inspiratory 
collapse. In apical tuberculosis a collection of delicate red or purple 
lines is commonly observed in the skin over the apex of the lung — the 
" striae vasculares" of Francke, attributed to permanent engorge- 
ment of the cutaneous blood-vessels due to toxins derived from an 
underlying focus of pulmonary infection. Lombardi has des- 
cribed as an early sign of apical phthisis the formation of small 
bluish varicosities near the lower cervical and the upper thoracic 
vertebral spines, and Sabourin has noted depressed ecchymotic 
spots in the dorsolumbar regions. The association of zona and of 
erythema nodosum with phthisis is a well-known clinical sign. 

Clubbed fingers, and perhaps true examples of Marie's osteo- 
arthropathy, are familiar findings during the later stages of the 
disease (See p. 123.) 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 



233 



Since tuberculous lesions produce x-ray shadows corresponding to 
their location, size, and density, the use of the fluoroscope and the 
radiograph is of real value in the diagnosis of phthisis, as well as in 
tracing its progress. In incipient cases haziness or mottling of an 
apex is shown by the fluoroscope, and in some instances a more or 
less disseminated darkening over the greater extent of the diseased 
lobe. Sometimes the shadows cast by a group of enlarged bron- 
chial glands give the first clue to the tuberculous process. The 
movement of the diaphragm is more restricted on the affected than 
on the sound side (Williams's sign), and, even in very early cases, 
inspiratory traction of the heart toward the diseased lung may be 
recognized. The "cough phenomenon," or the lightening of an 




Fig. 104. — Radiograph of phthisis (cf. Fig. 70). Early stage, showing apical infiltra- 
tion and glandular lesions. (Plate by Dr. W. F. Manges.) 

apicaf shadow as the subject coughs, does not. occur in. an infil- 
trated apex, but this change, which is due to full inflation of the 
lungs, is constant in health and in atelectasis of the apex. The 
practical utility of these findings, which may anticipate the other 
physical signs, is obvious, provided that they are correctly inter- 
preted. Failure to obtain an x-rav shadow from an incipient lesion 



234 



PHYSICAL DIAGNOSIS 



that affords clear physical signs occasionally is met with in recent 
infiltrations of very slight density. 

At a later period of the disease, when the tuberculous foci are denser 
and more wide-spread, their shadows are correspondingly deeper and 
more clear-cut, oftentimes because of their contrast with the excep- 
tional clearness of the neighboring emphysematous pulmonary tissue. 
A large cavity, if empty, produces a pale area, with peripheral darken- 
ing; if filled with -fluid, it casts a definite homogeneous shadow. 
Rontgen-ray examination does not reveal the presence of a small 
cavity in the midst of an area of fibrosis. The accompanying radio- 
graphs (Figs. 104, 105, and 106) serve to illustrate the shadows cast 
by various degrees of tuberculous infiltration. 

Palpation. — In early phthisis deficiencies of expansion so slight 




Fig. 105. — Radiograph of phthisis (cf. Fig. 70). Advanced stage, showing dense 
consolidation of right apex, with disseminated infiltration and fibrosis of both lungs. 
(Plate by Dr. W. F. Manges.) 



as to escape the eye are frequently appreciable by palpation, and this 
is true particularly of apical lagging, which is most readily detected 
by palpating the clavicular regions from behind, as elsewhere 
described. (See Fig. 75). 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 235 

Vocal fremitus is exaggerated over infiltrated areas not too deep 
seated, nor too effectually covered by emphysema, atelectasis, or 
thickened pleura. In view of the relative increase of vocal fremitus 
at the right apex, it follows that equal intensity of the fremitus at 
both apices denotes either undue increase on the left side or ab- 
normal decrease on the right. Other conditions being the same, 




Fig. 106. — Radiograph of phthisis (cf. Fig. 70). Far-advanced stage, showing 
dense infiltration of both lungs, especially at the apices. (Plate by Dr. W. F. 
Manges.) 



the more compact the infiltration, the better its conduction of the 
voice vibrations. Over an empty superficial cavity vocal fremitus 
is greatly magnified, but over one filled with liquid or having a 
plugged bronchial outlet the vibrations are entirely abolished. 
It is occasionally possible to feel succussion waves over a large, 
smooth-walled excavation containing thin fluid secretion. 

Mensuration and cyrtometry of the chest, save as a means of 
recording striking deformities, are generally dispensed with in the 
examination, of a phthisical, thorax, which in the advanced stages 
of the disease shows subnormal expansion, unusual measurements 
of the semicircumferences, and deviations from the normal depth 
and breadth. 



236 PHYSICAL DIAGNOSIS 

In many instances unilateral enlargement of the axillary and super- 
ficial cervical glands on the side of an apical lesion may be detected 
long before it becomes active. These glands, which Fernet believes 
to be affected secondarily to the pulmonary process, are small, mov- 
able, painless, and, strangely enough, tend to disappear as the primary 
infiltration of the apex lights up. Occasionally the subcutaneous 
lymphatic glands of the fourth and fifth interspaces in the axillary 
regions are distinctly palpable. Quite different from such indolent 
adenopathies are the soft, ulcerative forms of tuberculous adenitis 
which may serve as the determining factor of phthisis. 

Percussion. — The clavicular, supraspinous, and interscapular 
regions should be examined for the earliest indications of impaired 
resonance, which consist of a percussion sound of unduly high pitch 
and brief duration, associated with a sense of increased resistance 
over the part percussed. These evidences of moderate infiltration 
are gradually accentuated as the consolidation increases in density 
and in extent, until finally the sound becomes frankly dull and the 
resistance extreme. But every phthisical lung does not, during its 
incipient period, alter the percussion sound in this manner, for 
normal resonance, is not incompatible with a deep-seated compact 
infiltration, of considerable size entirely surrounded by healthy 
lung, nor with a superficial area of disseminated foci. The presence 
of an apical emphysema also is to be recalled as a potential factor 
of negativing the dulness of a consolidation in this region. In 
attempting to judge trifling apical differences it is important to 
draw conclusions after comparative percussion of the two sides, 
and sometimes impaired resonance of one apex is elicited only by 
respiratory percussion, while the subject holds the breath after a 
full inspiration. 

Apart from the demonstration of actual dulness at the apices, the 
attempt should be made to map out the respiratory rise of the lungs in 
these regions, by percussion over the supraclavicular regions from be- 
hind. (See Fig. 80, p. 141.) The roughly triangular area of pulmonary 
resonance, which normally extends \ to i| inches (1.25 to 3.75 cm.) 
above each clavicle (Philip), is more or less contracted by the lung 
shrinkage due to apical disease. (Cf. Kronig's isthmus, p. 144.) 
Especially significant of incipient phthisis, according to Minor, 
is a retraction, or outward dislocation, of the inner border of 
the apex, which, in health, runs upward from the sternoclavicular 
joint to a point if inches (4 cm.) internal to the free edge of the 
trapezius, and thence drops obliquely to the lower border of the 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 237 

second thoracic vertebra. Extraordinary skill in percussion is 
obviously necessary to detect this slight apical deviation. 

As the tuberculosis spreads through the lungs, the dulness corre- 
spondingly extends, acquiring, over areas of dense fibrosis and pleural 
thickening, a characteristic wooden quality quite different from the 
dulness of airless lung. In contrast to this, a decided hyperreso- 
nance may be found over a caseous infiltration undergoing rapid 
softening. 

A cavity affords either tympany or flatness, depending upon 
whether it be empty or filled with fluid. (See Fig. 83.) The "cracked- 
pot sound" and the amphoric " jug-sound" are also to be sought for, 
as well as the several special tonal changes described by Wintrich, 
Williams, Friedreich, and Gerhardt. (See p. 151 et seq.) In 
Landis's experience at the Phipps Institute, cavity tympany is 
elicited in about 70 per cent, of cases in which excavation exists. 
It is sometimes possible to empty an apical cavity by gently rapping 
upon the overlying chest-wall with a hard instrument, such as an 
ivory paper-knife, the effect being to excite a coughing fit which expels 
the secretion within the cavity and thereby develops cavernous signs — 
Erni's signe du tapotage. 

In most cases of phthises — and also in numerous other diseases — 
sharp immediate percussion of the upper anterior chest causes a pe- 
culiar muscular contraction, known as myoidema, appearing either 
as a hard, nodular swelling at right angles to the course of the muscle, 
or as a linear groove running in the direction of the muscular fibers. 

Auscultation. — Over a patch of beginning infiltration the inspiratory 
murmur may be either feeble and distant or loud and harsh, the former 
indicating imperfect entrance of air into the tuberculous area, and 
the latter, consolidation dense enough to conduct some of the bron- 
chial tone. The expiratory murmur is relatively rough, harsh, and 
prolonged. In incipient phthisis of the right apex J. S. Billings, Jr., 
finds that exaggerated respiratory and voice sounds are sharply 
restricted to the apex, while a similar intensification from physiologic 
causes is audible over the entire upper lobe. 

As the infiltration extends, the respiration becomes bronchovesicular, 
and finally bronchial, as the last vestige of the vesicular element is 
replaced by a tubular, blowing quality. Laennec's "veiled puff," 
recognized as an abrupt bronchial tone toward the end of an inspira- 
tion beginning as a vesicular sound, is a somewhat distinctive early 
sign; and respiration of the interrupted or "cog-wheel" type is quite 
common, though by no means pathognomonic of phthisis. Over 



238 PHYSICAL DIAGNOSIS 

parts of the lung affected by compensatory distention, exaggerated 
breathing is distinguishable. 

Over a cavity of fair size several modifications of bronchial breath- 
ing are audible, of which the hollow cavernous and the echoing 
amphoric types are the most distinctive; over a small cavity the breath- 
ing is more likely to be purely tubular. Seitz-metamorphosing res- 
piration, a tubulocavernous sound, usually inspiratory, is a less easily 
appreciable sign, occasionally heard over a cavity with a small bron- 
chial outlet. 

Vocal resonance is increased over infiltrated and excavated areas 
of the lung, and of the latter, whispering pectoriloquy is one of the 
most constant physical signs; it may, however, also be symptomatic 
of a dense peribronchial solidification. Clear pectoriloquy is very 
commonly heard in this condition when the stethoscope is applied 
to the tips of the upper thoracic vertebrae (see p. 308). 

Fine moist rales, pleural friction, and cavernous bubbling are the 
most pertinent adventitious sounds of chronic ulcerative phthisis. 
At an early stage moist bronchiolar subcrepitations, still finer vesicular 
crepitations, and delicate pleural friction-sounds are to be expected; 
or, should the bronchiolar mucosa be dry and swollen, piping sibilant 
rales are found rather than moist sounds, though the two are often 
intermingled. In some instances a single sharp mucous click is 
the first evidence of the tuberculous bronchiolitis. The foregoing 
rales are chiefly, if not altogether, inspiratory, and are usually much 
influenced by coughing and by deep breathing; their persistence at 
an apex is one of the earliest, most convincing indications of tuber- 
culosis in this region. Boeri advises auscultation immediately after 
active massage of the supraclavicular regions, as a means of identi- 
fying delicate apical crepitations otherwise inaudible; or they may 
be developed by instructing the patient to cough lightly at the 
end of expiration. 

If an area of pulmonary infiltration near the heart be forcibly 
jogged by the cardiac impact, audible vibrations may be set up in 
the exudate within the bronchioles and infundibula of the diseased 
area, thus producing so-called cardiac or cardiopneumatic rales. 
By a similar mechanism air may be driven from the finer tubes 
with an audible systolic whiff, known as a cardiorespiratory murmur. 

Pleural friction, which is generally demonstrable throughout the 
disease, may be restricted to the pleural layers overlying the heart, 
in consequence of which the sound conforms to the rhythm of pleuro- 
pericardial friction (q. v.). Pleural thickening, it is to be remem- 
bered, may be so extensive as to mask exaggerated fremitus, as well 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 239 

as to dull the percussion sound over an otherwise tympanitic area. 
Vascular murmurs, due to the pressure of a thickened pleura, are 
occasionally demonstrable over the subclavian arteries in tuber- 
culosis of the apex. 

As softening progresses and secretion accumulates within the 
larger bronchi, coarse mucous rales become audible, and, should dry 
bronchitis coexist in other parts of the tubes, snoring rhonchi are also 
heard. 

Over a cavity containing liquid there are various sized moist bub- 
bling and gurgling sounds of cavernous or amphoric quality, but a dry 
cavity affords no such physical signs. To cavernous rales, deep and 
active inspiration may add a sharp, clean-cut quality, described by 
Skoda as consonating or resonant, and metallic rales thus modified 
bear some resemblance to the metallic tinkle of hydrochorax, from 
which, however, they are readily distinguished by the associated 
physical signs. Exceptionally, a cavity of large size furnishes a 
succussion sound similar to the pleural splash. Cavernous rales 
may also be of the cardiopneumatic type, in case an area of con- 
solidation riddled with small cavities happens to be bound down to 
the heart by dense pleural adhesions. (See p. 170.) The trans- 
mitted sounds of the heart, and frequently of murmurs, should they 
exist, are clearly heard over large apical cavities. 

Under the term laryngeal crepitus Remouchamps describes a fine 
grating respiratory sound, detected, even in incipient phthisis, by 
placing the ear a few inches from the open mouth of the subject, 
who meanwhile breathes deeply, with the chin elevated and ex- 
tended. By this manceuver a bruit, comparable to the scratching 
of a pen upon a rough surface, is audible during respiration, espe- 
cially with expiration. The sound is due presumably to the laryn- 
geal amplification of adventitious sounds arising in the diseased 
tissues of the lung. 

Diagnosis. — No sign, however trivial it appears, should be dis- 
. regarded in the study of a case of possible incipient phthisis, for the 
diagnosis of which pulmonary physical signs alone may be wholly 
inadequate. Advanced cases, on the contrary, present no such diffi- 
culty, but a tuberculous lesion whose inroads afford convincing 
physical signs is correspondingly hard to arrest, and in such an event 
the physician may be able to do little save advise the patient to put 
his house in order against the inevitable finality. 

In some instances a beginning infiltration is betrayed by deficient 
expansion, exaggerated voice fremitus and resonance, a high-pitched 
percussion sound, an impure respiratory murmur, and a few fine 



240 PHYSICAL DIAGNOSIS 

moist rales over a circumscribed area, generally at an apex. In 
others there is merely an enfeebled or a harsh respiratory sound, 
with perhaps an occasional mucous click or a few subcrepitations. 
For the patient's sake, it is better to regard as tuberculous these 
evidences of a local bronchiolitis, if they persist at an apex, despite 
negative sputum examinations and an unaltered percussion sound, and 
in doubtful cases of this sort tuberculin may clear up the diagnosis 
at once. Aside from the local physical signs, it is essential to take 
into account many other evidences of the more or less active inroads 
of the tuberculous process — habitually rapid pulse, afternoon fever 
and shivering, spontaneous sweating, indolent adenitis, cough and 
huskiness of the voice, persistent nasopharyngeal catarrh, capricious 
appetite and chronic indigestion, slight secondary anemia, and pro- 
gressive languor and loss of weight. Very commonly the chief symp- 
toms are those of chronic bronchitis or of pleurisy, while sometimes 
hemoptysis is the first evidence found. Some patients exhibit an 
extraordinary degree of tolerance to the constitutional effects of the 
tuberculotoxin, and are not conscious of any decided ill health until 
the lungs have become extensively damaged; and in others the pul- 
monary lesions are overshadowed by symptoms relating to tuber- 
culosis of other parts of the body. 

In hilus tuberculosis (see p. 229) the subject, although obviously 
tuberculous, shows few definite physical signs, inasmuch as the 
lesion affects the deeper parts of the pulmonary structure where 
extensive damage is wrought before the surface is implicated. 
Save where the extension dominates one lung and pleura, thus ac- 
counting for unilateral restriction of expansion, the normal equality 
of the respiratory movements is preserved. The percussion find- 
ings relate to narrowing of Kronig's isthmus of apical resonance 
(q. v.); to bilateral dulness in the supra- and interscapular spaces 
(Riviere's "reflex bands of impaired resonance"); to right-sided 
paravertebral dulness; and occasionally to a parasternal patch 
of impaired resonance. Auscultation affords nothing distinctive 
until the late stages, when fine pleural friction and moist crep- 
itations appear at a base or in the axilla. The x-ray clearly 
reveals the central areas, accounting for the foregoing equivocal 
physical signs. 

Malarial fever may be simulated by phthisical attacks of chills, 
fever, and sweats, closely conforming to the paroxysms of ague, but 
the chest signs, the result of the blood and sputum examinations, and 
the patient's history furnish conclusive data for differentiating the 
two infections. 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 24 1 

Chronic bronchitis must be carefully distinguished from those 
forms of pulmonary tuberculosis having marked signs of bronchial 
implication. In ordinary chronic bronchial catarrh it is common 
to find the chest more or less emphysematous, with general hy- 
perresonance, diminished fremitus, feeble breath-sounds, greatly 
prolonged expiration, and numerous dry and moist bronchial rales 
of various size. 

The discrimination between bronchiectasis and a tuberculbus cavity 
is always difficult and frequently impossible. Basal cavity signs 
that persist without becoming exaggerated, paroxysms of coughing 
productive of fetid sputum containing no tubercle bacilli, absence of 
apical infiltration, and little or no disturbance of the patient's strength 
and nutrition are findings in favor of a non-tuberculous bronchial 
dilatation. The bronchiectatic "evacuative cough," which empties 
the cavity, must be distinguished from the phthisical " Morton's 
cough," which empties the stomach, often so repeatedly and effect- 
ually that the patient's nutrition suffers. 

A careful examination of the lungs is sufficient to identify cases of 
tuberculosis which masquerade as chlorosis, secondary anemia, and 
chronic gastric catarrh. Phthisis versus pulmonary abscess and 
gangrene is discussed elsewhere. (See p. 262.) 

FIBROID PHTHISIS (Tdberculofibrosis or Fibrotubercolosis of the 

Lungs) 

Clinical Pathology. — The predominant lesion in this variety of 
phthisis consists of a dense fibrous overgrowth whereby the tubercu- 
lous areas are compressed, encapsulated, and finally segregated or 
obliterated. The affection is one of decided chronicity, and develops 
apparently in subjects of great vital resistance, infected with tubercle 
bacilli of moderate virulence, owing to which conditions this con- 
servative cirrhosis destroys the tuberculous foci, limits their dissemi- 
nation, and in some instances effectually arrests the progress of the 
initial phthisical disease. In lungs cirrhosed in this manner the 
original tubercles are entirely effaced, or else are recognizable merely 
as encapsulated areas of sclerosis and as partly obliterated excava- 
tions. The latter, as in ulcerative phthisis, occasionally are of con- 
siderable size, and contain infective material which, in the course of 
time, may break through the cavity wall and contaminate the sur- 
rounding structures. Other cavities,, of smaller size, may be com- 
pressed into long, slender fistulous passages drained by neighboring 
bronchial tubes — the cicatrices fistuleuses of Laennec. 

Ultimately, the fibroid changes, although primarily reparative in 
16 



242 PHYSICAL DIAGNOSIS 

character, become so exaggerated as seriously to interfere with the 
pulmonary function, for they progressively encroach upon the alve- 
olar tissue, thus decreasing the respiratory area and exciting com- 
pensatory dilatation of the non-fibroid vesicles, and in time produce 
an extreme degree of induration and contraction of the pulmonary 
structure. In the event of extensive pleuropulmonary adhesion and 
contraction, conspicuous deformity of the thoracic wall develops. 

Fibroid phthisis is ordinarily a sequel of the chronic ulcerative 
type of the disease or of a tuberculous pleurisy, but it* may be secondary 
to other forms of tuberculosis of the lungs; or there may be a primary 
fibrosis, subsequently becoming tuberculous. The process usually 
implicates both lungs, and tends to become most extensive at one of 
the apices. Few sufferers from fibroid phthisis escape bronchiecta- 
sis, mainly because of the frequent incidence of dense fibrous 
adhesions which exert traction upon the bronchial walls. In con- 
sequence of the habitual obstruction to the pulmonary circulation 
that exists, cardiac hypertrophy, particularly of the right ventricle, 
sooner or later supervenes. 

Physical Signs. — Inspection. — The pulmonary contraction inevit- 
ably changes the contour of the thorax, drags the heart from its normal 
site, and disturbs the respiratory excursions, especially where the 
fibrosis is wide-spread and complicated by extensive pleural thicken- 
ing and by bronchiectasis. On the affected side, the respiratory 
movements are restricted, perhaps to the point of practical oblitera- 
tion, while the opposite half of the chest, provided that it has escaped 
extensive fibrosis, is vicariously enlarged. The thoracic wall is 
flat and depressed, either as a whole or locally; the shoulder droops; 
the clavicular areas are unduly deep; the interspaces are narrowed 
or even effaced by the crowding together and overlapping of the ribs; 
and the diaphragm is elevated above its normal level. In the extreme 
instance the spinal column inclines toward the shrunken side. The 
heart is usually drawn toward the affected area, the apex-beat being 
displaced toward the right axilla by fibrosis of the right lung, and 
toward the left axilla by a left-sided lesion ; in the latter the im- 
pulse of the heart is frequently visible upon the chest-wall from 
the second to the fifth interspaces. Owing to the enlargement of 
the right heart there are bulging of the lower part of the sternum 
and pulsation in the epigastrium and in the upper interspaces to 
the right of the sternum. 

Palpation. — The intensity of the local fremitis varies according 
to the character of the associated pulmonary and pleural lesions. 
Although the voice-sounds are clearly conducted by cirrhotic lung 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 243 

tissue, they are often diminished in fibroid phthisis, owing to the 
influence of pleural thickening, emphysema, bronchial obstruc- 
tion, and retraction of the lung from the chest -wall. Over apical 
cirrhosis there is usually exaggeration of the fremitus, but over a 
central lesion no such alteration is appreciable. 




Fig. 107. — Radiograph of fibroid phthisis. Extensive fibrosis of left lung, with corre- 
sponding cardiac displacement. (Plate by Dr. W. Manges.) 



Percussion. — Wooden dulness and a sense of extreme resistance 
to the pleximeter finger are elicited over the fibroid areas, especially 
when there are great pleural thickening and costal overlapping. 
Hyperresonance is the rule on the emphysematous side, as well as 



244 PHYSICAL DIAGNOSIS 

over circumscribed patches of overdistended lung adjacent to the 
seats of fibrosis. Circumscribed hyperresonance or pure tympany 
at the base of the lungs suggests an empty bronchial dilatation, 
and, at the apex, a pulmonary cavity. 

Auscultation. — Various degrees of bronchophony and bronchial 
breathing are audible, ranging from the slightly increased vocal 
resonance and bronchovesicular breathing of a partly cirrhosed area, 
to the clear pectoriloquy and bronchial or amphoric breathing of 
a compact fibrosis or of a cavity. Such changes are likely to be 
more marked at the apices than at the bases, where feeble respiration 
and many moist rales are ordinarily found. Other rales are also 
to be looked for, owing to the common association of bronchitis, 
tuberculous softening, and pleurisy. As the right heart dilates, the 
murmur of tricuspid incompetency appears, and the pulmonic second 
sound, previously accentuated and ringing, gradually weakens. 

Diagnosis. — With a deformed chest, cardiac displacement and 
right-sided enlargement, wooden dulness, intensified respiratory 
and voice-sounds, and signs of pulmonary softening or excavation, 
the diagnosis is generally clear. With nothing more than physical 
signs of fibrosis as a guide, the question of fibroid tuberculosis versus 
non-tuberculous interstitial pneumonia arises, and in making this 
distinction one is frequently forced to depend finally upon the results 
of sputum examination and the tuberculin reaction. The detection 
of bilateral lesions, together with the fact that the patient has or has 
had fever, sweats, loss of weight, and other suspicious systemic symp- 
toms, are suggestive of the tuberculous character of the process. 

PULMONARY SYPHILIS (Syphilitic Pneumonia or Fibrosis; White 
Pneumonia; White Hepatization of the Long; Pulmonary Albinism) 

Clinical Pathology. — Pulmonary syphilis deserves careful con- 
sideration, not on account of its common incidence, for it is rare, 
nor because of its distinctive physical signs, for there are none, but 
rather because of its close clinical resemblance to certain non-syphilitic 
affections of the bronchopulmonary system, from which the differen- 
tiation of true lues of the lung must be attempted. 

Gummata, interstitial fibrosis, and white hepatization of the 
vesicular structures are the essential pathologic changes of this rarely 
diagnosed condition, of which two sharply defined types, the acquired 
and the congenital, are generally recognized. In acquired syphilis 
of the lung the lesions are of gummatous and fibroid character, the 
former, though very rare, being by far the more distinctive of the two. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 245 

Although they may invade any part of the lung, gummata are most 
often situated toward the root, near the larger bronchi, or, indeed, 
these tubes may be directly implicated by tne granulomata, and in 
consequence are likely to become the seat of stenosis and of traction 
diverticula. Ordinarily, a gumma does not exceed 3 or 4 inches 
(7.5 to 10 cm.) in greatest diameter, and consists of a gray or yellowish 
caseous mass, inclosed by a fibrous capsule, either resilient and trans- 
lucent or rigid and dense, according to the age of the lesion. Necrosis 
and liquefaction of a gumma, with its rupture into a bronchus, leads 
to cavity formation, and absorption and cicatrization of the syphilitic 
focus results in scarring at its site. Interstitial fibrosis is sometimes 
associated, and, exceptionally, it appears to develop as a primarily 
leutic process, quite independent of gummatous growths. As a rule, 
the fibrosis begins at the root of the lung, and extends peripherally 
along the interlobular and interlobar septa, but occasionally it spreads 
in the reverse direction, being of pleurogenous origin. The con- 
dition is virtually a chronic interstitial pneumonia (q. v.), commonly 
of a lobar type, and attended by the pathologic changes in the vesic- 
ular structures, bronchi, and pleura incident to an ordinary cirrhosis 
of the lung. Acquired pulmonary syphilis may lack distinctive 
features, for a gumma may exactly resemble a caseous tuberculous 
mass, and a syphilitic cirrhosis does not differ from cirrhoses due to 
other factors. In the first instance the differentiation depends upon 
the presence of the tubercle bacillus, the syphilitic treponema almost 
never being found in a gumma; while in the second instance the 
most available differential criteria are the patient's history and the 
question of cutaneous scars and visceral lesions. Congenital syphilis 
of the lung is typified by a condition known as white pneumonia oj 
the fetus, characterized by hyperplasia of the intervesicular walls 
and proliferation of the cells lining the vesicles, with consequent 
obliteration of the vesicular structure through various areas, scattered 
or diffuse, of the lung or lungs. The affected parts teem with Trepo- 
nema pallida, and, owing to the hyperplasia, become anemic, airless, 
and consolidated, being distinguishable as firm, non-crepitant, 
grayish-white territories, described as white hepatization of the lung. 
White pneumonia is found in the fetus, in still-born infants, and 
in those born alive, but in the last named no stress of respiratory 
effort, however strong, is sufficient to inflate the consolidated 
areas. Gumma affects the congenitally syphilitic lung but very 
rarely. 

Physical Signs and Diagnosis. — That acquired syphilis of the 
lung is attended by no distinctive thoracic signs must be apparent 



246 PHYSICAL DIAGNOSIS 

when the nature of the several pulmonary lesions is considered. 
According to the conditions predominating in the individual case, 
the physical signs ordinarily suggest chronic ulcerative phthisis, 
bronchostenosis, bronchiectasis, or pulmonary fibrosis. 

Phthisis is counterfeited, not alone by signs of consolidation and 
perhaps of excavation, but also by the occurrence, with greater or 
less constancy, of cough, dyspnea, mucopurulent and bloody sputum, 
pleural pain, night-sweats, and emaciation. These last three symp- 
toms are, however, comparatively infrequent, and, when present, 
are usually not striking — a circumstance of some consequence in 
favor of lues. But of far greater suggestiveness is the fact that the 
sputum invariably remains free from tubercle bacilli, in spite of its 
apparently tuberculous appearance and notwithstanding, in many 
instances, the clinical evidences of advanced consumption. Appar- 
ently, true syphilis organisms are never found in the sputum, judging 
from Rosenberger's analysis of 12 10 collected cases. The reputed 
tendency of syphilis primarily to affect the middle lobe of the right 
lung, and the predilection of the right apex for tuberculous infection, 
are of minor, but not wholly negligible, significance. If the patient 
in past years has sown the wind so as now to reap a luetic whirlwind, 
syphilis, rather than tuberculosis of the lungs, is strongly suggested, 
this inference becoming the stronger if it be possible to identify the 
scar of the initial lesion, and to find signs of arteriosclerosis and of 
syphilitic processes elsewhere. Finally, so far as phthisis is concerned, 
the diagnosis may be settled by the tuberculin test: if positive, the 
lesion is tuberculous, though, unfortunately, this does not necessarily 
rule out coexisting syphilis of the lung; but a negative reaction with 
tuberculin excludes phthisis, and by the same token indicates syph- 
ilis — beyond all question if it be associated with a strongly positive 
Wassermann reaction. If tempted to use potassium iodid as a 
therapeutic test, one should weigh the baneful effects of this drug 
in lighting up a tuberculous process against its action in subduing 
lues. Much the better plan is to anticipate improvement under 
the use of salvarsan. 

Bronchial stenosis, due to the encroachment of gummatous nodules 
or to stricture by scar tissue, must be distinguished from bronchial 
occlusion by aneurism and by malignant tumor, especially sarcoma. 
Aneurismal pressure generally can be definitely proved with the ai4 
of the .T-ray , even if the classic physical signs of this lesion be lacking. 
(See Aneurism, Section VI.) A history of syphilis and the existence of 
arteriosclerosis, it should be noted, favor aneurism as well as gumma. 
The following points are in favor of sarcoma rather than gumma : signs 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 247 

of consolidation in the anterior mediastinum prior to the onset of the 
bronchial obstruction; rapidly developing and often conspicuous 
symptoms, referable chiefly to the mediastinal vascular trunks and 
nerves; initial or secondary metastatic growths in parts remote from 
the thorax; anemia or cachexia of the patient, a clean personal history, 
and no scars or other relics of syphilis; and an unaltered clinical 
picture, despite the subject's saturation with iodids and mercury. 
Here also the .T-ray may be of service, both in making the initial 
diagnosis and because of the fact that sometimes malignant growths 
diminish extraordinarily under persistent rontgenization, while gum- 
mata do not. 

The physical signs of syphilitic bronchiectasis are in no wise dis- 
tinctive, so that its differentiation from bronchial dilatation due to 
other causes rests upon other clinical evidence. The same is true 
of syphilitic fibrosis of the lung and its attempted discrimination 
from other types of chronic interstitial pneumonia. 

Congenital syphilis of the lung is usually revealed only at autopsy, 
inasmuch as it is prone to affect still-born infants or those dying soon 
after birth. Occasionally white pneumonia is suggested by finding 
consolidative and other evidences of bronchopneumonia in a young 
baby showing unmistakable stigmata of congenital syphilis. 

EMPHYSEMA 
The word emphysema, literally meaning inflation, is applied, with 
an appropriate adjective, to several distinct, but frequently inter- 
dependent, pulmonary lesions of widely diverse character, affecting 
the vesicular and interstitial structures, either singly or together. 
Of the vesicular type of emphysema there are, according to current 
clinical nomenclature, four varieties : the hypertrophic or large-lunged, 
or a condition of chronic vesicular dilatation and septal wasting 
eventually leading to increased pulmonary volume; the atrophic or 
small-lunged, characterized by extreme and progressive atrophy 
of the vesicular structures, resulting in diminution of the pulmonary 
volume; the acute vesicular, in which a widely diffused overdistention 
of the lungs suddenly develops; and the compensatory, or a more or 
less circumscribed overinflation of the vesicles, either acute or chronic 
in character, and not primarily attended by permanent structural 
damage. The term interstitial emphysema is used to designate an 
accumulation of air in the interstitial connective tissues of the lung. 



248 



PHYSICAL DIAGNOSIS 



HYPERTROPHIC EMPHYSEMA (Large-lunged, Pseudohypertrophic, Sub- 
stantive, True, or Idiopathic Emphysema; Alveolar Ectasia) 

Clinical Pathology. — In this type of emphysema the lungs are 
permanently overinflated as the result of impaired pulmonary elastic- 
ity, combined with a state of persistent intravesicular hypertension 
(Fig. 1 08). The use of the adjectives hypertrophic and pseudo- 
Large bulla 



Emphysematous 
border of lung -< 




Large bulla 
Fig. 108. — Pulmonary emphysema (Jefferson Hospital Laboratories). 



hypertrophic to denote this form of emphysema relates merely to 
the enlarged volume of the lungs, and not to the predominant tissue 
changes, which are essentially atrophic. Impaired pulmonary 
elasticity may be an hereditary taint, whereby the elastic tissue of the 
lungs is inherently deficient or subnormally resistant; or the defect 
may be acquired through damage by processes inducing degeneration 
and atrophy of the elastic fibers, such as, for example, chronic bron- 
chial catarrh, atheroma, and similar factors of disordered nutrition. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 249 

Given a predisposition of this sort, increased intravesicular pres- 
sure, especially when due to expiratory strain or overdistention, 
acts as the determining cause of emphysema. Emphysema is 
directly related to impaired alveolar ventilation, with an increase 
in the dead space of the lungs due chiefly to atonic elongation and 
broadening of the bronchioles and, in part, to bronchiolar spasm 
(Hoover) . 

Expiratory overdistention of the vesicles, the ruling factor in most 
cases, attends violent expiratory efforts associated with obstruction to 
the free outlet of the air-columns. Thus, in paroxysms of coughing the 
closure of the glottis plus the active pressure of the chest- wall together 
provoke inordinate tension within, and undue stretching of, the air-vesi- 
cles, especially toward the apices and along the anterior margins of the 
lungs, where the pulmonary structure, being poorly supported by the 
parietes, becomes the natural target of the violent gusts of air which, 
owing to the closed glottis, cannot escape by their natural channels. 
The poor support afforded by the intercostal muscles possibly has 
something to do with the development of emphysema in other por- 
tions of the lungs, which are successively approximated to the yielding 
interspaces 'during the progressive emphysematous changes in costal 
contour. Chronic bronchitis, asthma, and pertussis, chiefly in that 
they excite extreme intravesicular tension during expiration, are 
prominent causes of emphysema. In the light of modern studies 
(by Schmidt, Prettin, and others) the old belief that glass-blowers 
and players of wind instruments are peculiarly prone to emphysema 
must be regarded as a medical tradition. 

Inspiratory overdistention of the vesicles apparently has little, if 
any, bearing upon the production of true large-lunged emphysema, 
though it is a most potent factor of the so-called compensatory 
variety (q. v.) . It is, however, conceivable that a variable degree of 
vesicular dilatation might arise should relatively excessive inspira- 
tory movements and shallow, imperfect expiration coexist, as is 
the tendency when the thoracic resiliency is impaired by age or by 
disease. 

Postmortem, the distinguishing marks of emphysematous lungs 
are their immoderate bulk, diminished weight, pale appearance, 
and disinclination to collapse; they convey a peculiar feathery sen- 
sation when handled, and their borders extend far beyond the normal 
limits, conspicuously encroaching anteriorly upon the cardiac and 
the hepatic areas. The emphysematous tissue fails to crepitate, 
pits easily on pressure, and is recognized beneath the pleura as a 
series of globular or irregular bullae, ranging in size from a few milli- 
meters to several centimeters, and, as a rule, attaining their maximum 



250 PHYSICAL DIAGNOSIS 

development along the anterior inferior margins, at the root of 
the lower lobes, and at the apices of the lungs. Fig. 108 shows 
the appearance of these large emphysematous air-bladders along 
the pulmonary borders. On cross-section of a dry inflated speci- 
men, the lung is found to be riddled with these enlarged vesiculo- 
infundubular compartments, both single and multilocular, formed 
by the rupture and coalescence of numerous individual over- 
distended vesicles. Microscopically, the changes relate to atrophy, 
thinning, and perforation of the intervesicular walls, obliteration 
of the capillary network therein, quantitative and qualitative deterio- 
ration of the elastica, and degeneration of the alveolar epithelium. 
Bronchitis and peribronchial thickening are virtually constant, and 
ectases of the finer bronchi are frequent associated changes. The 
pleura is generally dry and pale, and may show the white patches 
of Virchow's "pulmonary albinism." The rupture into the pleural 
cavity of an emphysematous bulla may set up pneumothorax. Owing 
to the stress imposed upon it by the impeded pulmonary circulation, 
the right side of the heart undergoes hypertrophy and dilatation, 
and occasionally a general cardiac enlargement supervenes; the pul- 
monary artery may be dilated and atheromatous. Various organs, 
notably the liver, spleen, and kidneys, show the familiar structural 
changes induced by chronic venous congestion. 

Physical Signs. — Inspection. — The permanently overinflated 
"barrel chest," described in a preceding section (see p. 80), is dis- 
tinctive of advanced cases of many years' development, although this 
deformity is by no means invariable. In certain subjects the costal 
cartilages are abnormally thickened and lengthened, corresponding to 
the " specific calcification " exploited half a century ago by Freund, as 
a primary and specific emphysematous change. Dyspnea, cough, 
cyanosis, and clubbing of the finger-tips are important objective signs 
which become more and more marked as the disease advances, with 
consequent loss of pulmonary elasticity, restriction of the respiratory 
surface, defective blood aeration, and exaggeration of the bronchitic 
lesions. When the right heart fails under the stress of the intrapul- 
monary hypertension, these signs become most striking, and are 
attended by jugular pulsation, general venous turgescence, and edema. 
Epigastric pulsation, due to the movements of a displaced and 
enlarged heart, is common, but the true apex-beat is obscured by 
the interposed mass of emphysematous lung. During respiration 
the thorax rises and falls en masse in a vertical direction, but fails 
to expand normally, despite the strenuous attempts of the aux- 
iliary muscles to overcome the rigidity of the chest-walls. Litten's 
shadow begins at a lower level and is shorter than in the healthy 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 25 1 

chest, owing to the abnormally low position and limited mobility 
of the diaphragm. In the exceptional instance this muscle is so 
extremely depressed and relaxed that its convexity lies toward 
the abdomen instead of toward the thorax. This inverted position 
of the diaphragm, whereby it serves as an expiratory rather than 
as an inspiratory muscle, gives rise to what is termed an inverse 
type of respiration. The fossae above the clavicles and sternum and 
the upper intercostal spaces may be sucked in with deep inspiration, 
while the lower interspaces tend to become obliterated, or even to 
balloon outward, during expiration. Sudden inflation of both supra- 
clavicular spaces sometimes accompanies a coughing fit severe enough 
violently to distend the air- vesicles of the apices. 

Palpation. — Bilateral enfeeblement of vocal fremitus is a character- 
istic tactile finding, its principal factors being the indifferent con- 
ducting properties of the lung, diminished resiliency of the thorax, 
and occlusion of the bronchi by secretion and by mucosal swelling. 
In some instances these causes, singly or combined, are capable of 
entirely cutting off the transmission of voice vibrations to the chest- 
wall. When decided bronchial catarrh coexists, there is rhonchal 
fremitus. Ordinarily the apex-beat is impalpable at its normal 
site, but the systolic impulse of the right ventricle can be felt in the 
epigastric region. Both the liver and the spleen may be so large 
and depressed as to be readily palpable below the costal margin, 
and over the former, in the event of extreme dilatation of the right 
heart, venous pulsation is occasionally appreciable. Localized 
tenderness and pain in the region of the xiphoid is common, this so- 
called " epigastric spot '"of pain being attributable to undue pressure 
within the right ventricle. 

Percussion. — The percussion sound is loudly hyperresonant and 
the resistance generally is increased over the greater part of both 
lungs, but especially over the upper lobes anteriorly are these char- 
acteristics most clearly demonstrable. Strictly speaking, the sound is 
not a pure tympany, but rather tympany ingrafted upon a box-like 
tone — Biermer's "band-box resonance," or a commingling of vesicular 
resonance and tympany — Flint's "vesiculo tympany." Percussion of 
the pulmonary borders at the apices, bases, and precordia shows that 
the unnatural resonance extends far beyond the normal limits of the 
lungs, and comparative percussion at the base reveals little or no 
inspiratory-expiratory difference in the levels of the pulmonary 
borders, indicating restricted excursion of the emphysematous 
lungs. The encroachment of the hyperresonance diminishes or 
entirely obliterates cardiac dulness, lowers the upper levels of the 



252 PHYSICAL DIAGNOSIS 

hepatic and splenic areas, and extinguishes the pure gastric tym- 
pany of Traube's space. 

Auscultation. — Enfeeblement of respiratory murmur, with low- 
pitched and notably prolonged expiration and short, silent inspira- 
tion, is the distinctive auscultatory finding. Expiration, whose 
duration equals or exceeds that of inspiration, may be either almost 
inaudible, or, if bronchitis and asthma coexist, wheezy, harsh, and 
more or less masked by bronchial rales. Over the distended areas 
where the pulmonary elasticity persists the breath-sounds are vicari- 
ously exaggerated and puerile in character. Vocal resonance 
behaves like vocal fremitus (v. s.). A peculiar parchment-like 
crepitation, audible chiefly at the apices during forced inspiration, 
has been described in emphysema, the production of the sound being 
variously referred to the friction between subpleural bullae and the 
costal pleura and to the crackling expansion of the emphysematous 
tissue, of which factors the former appears the more plausible. As 
the result of right heart failure, the liquid bubbling of pulmonary 
edema may be detected at the bases posteriorly. The cardiac sounds, 
owing to the interposed lung, are distant and muffled, and with the 
supervention of leakage at the right auriculoventricular orifice, a 
systolic murmur in the tricuspid area develops. The pulmonic 
second sound is accentuated during the phase of right ventricular 
hypertrophy, but weakens progressively as this chamber becomes 
inadequate and finally dilates. 

Diagnosis.— Habitual cough, dyspnea, and cyanosis with bilateral 
thoracic distention, hyperresonance, a vertical type of respiration, 
and unduly prolonged low-pitched expiration admit of but one 
interpretation. 

Simple chronic bronchitis, while it may give rise to cough, dyspnea, 
and somewhat prolonged expiration, is not attended by enlargement 
and increased resonance of the thorax, so long as it is unaccom- 
panied by emphysema. 

Pneumothorax, like emphysema, is attended by cough, labored 
breathing, and signs of defective blood aeration, but in the former 
the attack is most sudden and its severity most alarming, while in the 
latter the symptoms develop gradually and are not so urgent. The 
physical signs of pneumothorax differ from those of emphysema in 
being unilateral, not bilateral; the increased resonance more often 
amounts to pure tympany than to ordinary hyperresonance; the 
respiratory and voice-sounds, if not wholly abolished, are amphoric 
and echoing, instead of being merely enfeebled or wheezy. More- 
over, air within the pleural cavity causes most conspicuous visceral 
displacement, and, when associated with a liquid effusion, is betrayed 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 253 

by several distinctive signs— Hippocratic succussion sound, metal- 
lic tinkling, and basal flatness. Should air escape into the pleural 
cavity from an emphysematous lung, the physical signs of the latter 
condition will be suddenly replaced, on the side of the pleural per- 
foration, by those of acute pneumothorax. 

ATROPHIC EMPHYSEMA (Small-lunged Emphysema; Senile Atrophy of the 

Lungs) 

This affection is essentially a senile atrophy of the lungs, which 
eventually shrink to a surprisingly small volume, and are converted 
into a mass of atrophic, functionless tissue permeated by air-spaces 
of various size, constructed o f dilated, wasted, and ruptured infundib- 
ula and air-vesicles. The atrophied lungs are commonly the seat 
of deep pigmentation, and are not infrequently affected by local 
fibrosis, congestion, edema, and infarction. Progressive atrophy 
of the thoracic muscles accompanies the pulmonary wasting, until 
finally the chest, in strong contrast to that of hypertrophic emphy- 
sema, becomes abnormally small, and the course of the ribs extremely 
oblique, thus diminishing the thoracic diameters and capacity, and 
creating an acute subcostal angle; the respiratory movements are 
about equally restricted during both phases of respiration. The 
heart, like the lungs, is atrophied — it is not subject to undue stress, 
and, therefore, neither hypertrophies nor dilates. 

The physical signs differ somewhat in detail from those of large- 
lunged emphysema. The dyspnea is inspiratory-expiratory, not 
chiefly expiratory; vocal fremitus is more likely to be exaggerated 
than enfeebled; the hyperresonance is often modified by fibroid 
deposits at the apices and by congestive and edematous changes at 
the bases. Owing to the pulmonary shrinkage the limits of the lungs 
are contracted, and in consequence there is an apparent increase in 
the extent of the cardiac and hepatic dulness, though both the 
heart and the liver actually may be smaller than normal. 

The diagnosis of atrophic emphysema usually can be made at 
a glance, by noting the size and shape of the thorax and the evidences 
of senile changes elsewhere. Chronic cough and moderate dyspnea 
attend the development of the atrophic alterations. 

COMPENSATORY EMPHYSEMA (Collateral, Complementary, Vicarious, 
or Local Emphysema) 

When a circumscribed part of the lung is rendered impervious to 
air, other areas suffer undue inspiratory distention, in an endeavor 
to compensate for the loss of aerating surface in the crippled part, 
and the overinflated pulmonary tissue upon which this extra work 



254 • PHYSICAL DIAGNOSIS 

is imposed is said to be in a state of compensatory, complementary, 
or vicarious emphysema. The distended vesicles contain a consider- 
able excess of air, and it frequently happens that this excess is not 
entirely expelled by the expiratory efforts, owing to some bron- 
chiolar obstruction, by secretion or by a turgid mucosa, sufficient 
to prevent the free exit of air, but not necessarily interfering with its 
entrance. Thus, the intravesicular tension becomes progressively 
increased, and the air-cells more and more stretched, until, finally, 
should the underlying cause persist, permanent dilatation, with 
structural changes like those of true hypertrophic emphysema, is 
established. If, on the contrary, the factor of this vicarious distention 
is removed before the pulmonary elasticity is impaired and the 
vesicles irreparably damaged, their temporary overinflation entails 
no subsequent derangement of function. 

Circumscribed vesicular dilatation takes place in the sound lung 
adjacent to areas of atelectasis, fibrosis, tuberculosis, and other 
lesions provocative of local airlessness of the pulmonary tissues, and 
in wide-spread adhesive pleurisy a corresponding degree of vicarious 
dilitation exists, especially along the anterior borders of the lungs. 
Compensatory emphysema of an entire lung is usually traceable to 
extensive cirrhosis, large pleural effusion, massive pneumonia, or 
pneumothorax of the opposite lung. As already intimated, the 
extent, character, and permanence of a compensatory dilatation of 
the lungs stands in direct relation to the nature and the duration of 
the underlying cause. 

The physical signs over the affected area or areas vary with the 
extent of the process and the structural alterations wrought thereby. 
If there be simple acute dilatation with increased elasticity of the 
lung, as is often the case, hyperresonance, a harsh puerile respiratory 
murmur, with little or no prolongation of its expiratory phase, and 
exaggeration of vocal fremitus and resonance are the findings. If 
the process be of longer standing, impairing the contractile power of 
the lung, the signs are similar to those of generalized hypertrophic 
emphysema, restricted to the part implicated. The diagnosis 
depends not so much upon these signs, which, unfortunately, are 
in many instances obscure, as it does upon the patient's history and 
the detection of some satisfactory cause of the compensatory process. 

ACUTE VESICULAR EMPHYSEMA (Acute Pulmonary Distention) 

In certain cases of urgent dyspnea a sudden bilateral hyperdis- 
tention of the lungs sometimes occurs, due in part to excessive inspir- 
atory stretching of the vesicles and in part to expiratory stress. The 
condition is one of simple functional pulmonary distention unat- 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 255 

tended by atrophic changes in the vesicular walls, the increased 
volume of the lungs depending entirely upon a generalized dilatation 
of the air-cells. This so-called acute vesicular emphysema may 
develop, with striking abruptness, during acute diffuse bronchitis, 
bronchial asthma, pertussis, or cardiorenal disease, and in tracheal 
and laryngeal stenoses. The sprinter's " second wind, " says White- 
locke, is presumably an acute type of physiologic emphysema, due 
to violent exercise. The physical signs are similar to those of hyper- 
trophic emphysema, save that the right heart shows no evidences 
of habitual strain. (Cf. Acute Pulmonary Tympanites, p. 149.) 

INTERSTITIAL EMPHYSEMA (Interlobular or Intervesicular Emphysema) 

Interstitial emphysema, or an accumulation of air in the stroma 
of the lung, arises when, in consequence either of trauma or of violent 
expiratory strain, air escapes through a breach in the intervesicular 
walls into the intervesicular and interlobular tissues, where it collects 
in the form of bubbles ranging in size from about a millimeter to a 
centimeter or larger. These bubbles of air, if not absorbed, may 
work through the interstitial tissues to the surface of the lung, where 
they persist as little globules or as larger bullae, freely movable 
beneath the pleura; exceptionally, the air burrows from the root of 
the lung into the mediastinum and thence upward along the trachea 
into the subcutaneous structures of the neck and the thoracic wall; 
or — and this also is uncommon — the pleura may be perforated and 
spontaneous pneumothorax produced. Air entering through a 
tracheotomy wound sometimes travels downward through the peri- 
tracheal and peribronchial tissues, ultimately collecting in the sub- 
pleural connective tissue. Apart from that variety due to wounds 
of the lung, interstitial emphysema is referable to alveolar rupture 
caused by violent fits of coughing, and by the excessive intrapulmonary 
tension incident to convulsions, parturition, and straining at stool. 

Physical signs of interstitial emphysema are usually lacking, and 
the condition is discovered more often at autopsy than clinically. 
When the cellular tissue of the neck is infiltrated with air, one some- 
times detects a subcutaneous emphysematous swelling which, on 
palpation, affords a curious sort of crackling sensation, while it has 
been asserted that a peculiar " crumpling friction-sound" can be 
heard over a collection of subpleural beads of air. 

ATELECTASIS (Pulmonary Collapse; Apnettmatosis) 

Clinical Pathology. — Atelectasis, or collapse of the lung, is met 
with either as an acquired condition or as a congenital defect, the 
latter being of but little interest to the internist. Acquired atelectasis 



256 PHYSICAL DIAGNOSIS 

is due to factors depriving the lung of its normal content of air and 
effectually preventing its reinflation, eithei by obstructing the passage 
of air through the bronchi, by actual compression of the pulmonary 
structure, or by persistent inadequacy of expansion. Obstruction 
atelectasis is secondary to bronchial obstruction with absorption 
of the air in the vesicular territory beyond, and this type of pulmo- 
nary collapse is referable to occlusion of the bronchial lumen by 
mucosal swelling, viscid secretion, membrane, blood-clot, calculus, 
aspirated foreign bodies, cicatrices, and new-growths; or bronchial 
stricture due to external pressure, glandular, neoplastic, or aneuris- 
mal, may be the underlying cause of the atelectatic lesion. Com- 
pression atelectasis arises when the lung is subjected to pressure, 
such as that exerted by large pleural and pericardial effusions of 
liquid, pneumothorax, hypertrophy of the heart, and aneurism or 
morbid growth of the thorax; less commonly the pressure is sub- 
phrenic, as in the case of a large abdominal tumor or effusion, whereby 
the diaphragm is displaced upward and crowded against the pul- 
monary bases; and in the exceptional instance the compression is 
traceable to a crooked spine or to a deformed chest- wall. A variable 
degree of atelectasis, from habitual vesicular underinflation, also 
attends inadequate expansion of the lungs, whether due to simple 
shallow breathing, to prolonged dorsal decubitus, or to diminished 
irritability of the respiratory center. 

Congenital atelectasis, met with in prematurely born and in weakly 
full-term infants, is characterized by imperfect inflation of the lungs 
after birth, owing to feeble respiratory movements or to bronchial 
occlusion by aspirated secretion. This type of vesicular collapse is 
either disseminated in numerous areas throughout both lungs, or 
implicates the greater part of a lobe or even of an entire lung, in the 
last event meriting the title apneumatosis. 

The appearance of an atelectatic lung varies with the extent and 
the chronicity of the process (Fig. 109). Multiple small foci of 
collapse, such as those incident to catarrhal pneumonia, show beneath 
the pleura as depressed blue or purple spots, each surrounded by 
a paler zone of vicariously dilated vesicles. An extensive area of 
diffuse collapse, due, for example, to the pressure of a large pleural 
effusion, consists of tough, dense, airless tissue, gray or of a light pink 
hue, and perhaps limited and bound down by fibrous bands and by 
a thickened, contracted pleura. The lung above the seat of atelectasis 
is compensatorily distended, and should the collapse be wide-spread, 
the lung is pushed upward and backward against the spinal column. 
If the cause be speedily removed and no inflammatory complications 
develop, the atelectatic area or areas may reinflate and the normal 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 



257 



function of the vesicles be completely restored, but if the collapse 
persists, irreparable damage to the lung occurs, and the deflated part 
becomes permanently deprived of air. In the latter event the com- 
pressed and intimately opposed intervesicular septa undergo infiltra- 
tion with blood, whereby the affected part is converted into a dark, 





Bronchi 



Atelectatic and carnified area 
Fig. 109. — Pulmonary atelectasis (Jefferson Hospital Laboratories). 

pulpy patch of splenization ; later the epithelium of the air-cells degene- 
rates, and the vesicles become coalescent and matted together by 
newly proliferated cellular tissue until, finally, the atelectatic focus 
is transformed into a mass of the consistence and general appearance 
of raw beef — pulmonary carnification. Subsequently this carnified 
tissue organizes, forming in the course of time a firm, contracted, 
pigmented patch of cirrhosis. As a rule, there are thickening and 

adhesion of the pleurae adjacent to an atelectatic lesion, and the 
17 



258 PHYSICAL DIAGNOSIS 

bronchial tubes passing through it are inflamed, dilated, and other- 
wise altered structurally. 

Physical Signs. — The physical signs of atelectasis are intimately 
blended with those of the exciting cause of the change, as, for example, 
the coexisting catarrhal pneumonia, pleural effusion, or enlarged 
heart, and, furthermore, they are determined by the extent and the 
situation of the atelectatic area, as well as by the secondary changer 
existing therein and in the adjacent lung. 

Inspection. — In extensive atelectasis there is extreme respiratory 
distress, as shown by the subject's rapid, shallow breathing, cyanosis, 
and inspiratory recession of the lower thorax and epigastrium. 
Indeed, in many instances these dyspneic phenomena are practically 
all that one finds, for deeply seated areas of collapse, if not far beyond 
the range of percussion and auscultation, produce signs whose identity 
is masked by the attendant compensatory emphysema and bronchial 
sounds. 

Palpation. — Collapsed, toneless pulmonary tissue, being a poor 
conductor of vibrations, weakens vocal fremitus, but when the deflated 
area undergoes consolidation and becomes denser, the fremitus if, 
clearly transmitted if not exaggerated. Pleural friction sometimes 
may be felt when the condition of the pleurae is such that they grate 
noisily with the respiratory excursions. 

Percussion. — As a rule, there is nothing more than emphysematous 
hyperresonance, save in the case of a circumscribed compact lesion 
near the surface of the lung; this, of course, impairs pulmonary 
resonance, and sometimes affords typical dulness, with undue plexi- 
meter-finger resistance. If tightly compressed against a large patent 
bronchial tube, a large patch of atelectatic lung may give a tympanitic 
note, since, to all intents and purposes, the bronchus is an air-con- 
taining cavity, whose tone traverses, unaltered, the adjacent dense 
and airless pulmonary tissue. 

Auscultation. — The respiratory murmur is generally suppressed, 
or quite lost, but over a dense peribronchial patch bronchovesicular 
or typical bronchial breathing may be heard. Provided that some 
air enters the collapsed vesicles, a few crepitant and subcrepitant 
rales are audible toward the end of deep inspiration. In bed-ridden 
subjects, with no pulmonary disease, atelectatic crepitations over the 
bases and the anterior borders of the lungs are very common, as the 
result of prolonged recumbency which, by interfering with adequate 
vesicular inflation, has allowed collapse and mural agglutination 
of some of the air-cells. With deep inspiration, however, the col- 
lapsed vesicles inflate, with the production of audible crepitations 
as their sticky walls separate. (See p. 168.) 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 259 

Diagnosis. — As a foregoing paragraph suggests, in many instances 
the diagnosis of atelectasis must needs be inferential rather than 
evidential, being based upon such findings as respiratory distress, 
hyperresonance, and signs of some condition causative either of bron- 
chial obstruction or of pulmonary compression. Small foci of col- 
lapse, even if numerous, give no tangible symptoms whatever so 
long as they are well compensated by the coexisting vesicular dilata- 
tion. A dense circumscribed area of atelectasis furnishes the signs of 
consolidation — exaggerated fremitis, bronchophony, harsh or tubu- 
lar respiration, and dulness, if the communicating bronchi remain 
open; respiratory silence and dulness, if the bronchi be plugged. 

Here may be noted the lesion of acute lobar atelectasis, due to 
diphtheritic paralysis and to reflex inhibition of the phrenic move- 
ments after surgical operations ; less commonly acute lobar collapse 
results from pneumothorax and from obstruction of the air-pas- 
sages. In this "active lobar collapse of the lung," described 
by William Pasteur, the main features include the abrupt on- 
set of dyspnea, cyanosis, and thoracic pain attended by moder- 
ate cough and considerable greenish sputum; the physical signs 
point to unilateral lobar collapse, associated with a notable 
dislocation of the heart toward the affected side. As a rule, these 
active symptoms persist for but a brief period, and the deflated 
lung regains its former functionating power within a few days. 

Atelectatic solidification is differentiated from croupous pneu- 
monia by the absence of a distinctive pneumonic symptom-com- 
plex, and by contrasting the history and course of the two affec- 
tions and the associated pulmonary changes incident thereto. 

PNEUMONOCONIOSIS 

Clinical Pathology. — A combined fibrosis and pigmentation of 
the lungs, due to the inhalation of minute particles of dust, is known 
as pneumonoconiosis, of which general process there are numerous 
special types, corresponding to the character of the aspirated material. 
Thus, antkracosis (coal-miner's lung; black phthisis) is common 
among miners and stokers, w T ho habitually breathe an atmosphere 
heavily charged with pulverous carbon (Fig. no). Siderosis (knife- 
grinder's phthisis; grinder's asthma) results from the inhalation of 
fine particles of metal, especially iion and steel; this form of pneu- 
monoconiosis particularly affects grinders and polishers, who 
are exposed to the clouds of metal dust produced by the abrasion 
of metallic surfaces by a grindstone. Chalicosis or lithosis (grinder's 
rot; stone-cutter's phthisis) is due to the inhalation of mineral dusts 



260 



PHYSICAL DIAGNOSIS 



inseparable from the trades of stone-cutting, dressing, and polishing ; 
to some extent those who suffer from siderosis also acquire more or 
less chalicosis, from breathing the fine dust abraded from the sur- 
face of the grindstone. Kaolinosis (potter's lung) develops from the 
aspiration of the dust of kaolin, a plastic clay used in making pottery. 
Millers, as well as those who handle tobacco, cotton, flax, furs, and 
other organic materials, are subject to inhalation cirrhoses from dust 
irritation. Of the preceding varieties of pneumonoconiosis, that 
due to soot or coal-dust is the least destructive, and though a miner's 
lung may be densely carbonized throughout, severe structural changes 
do not necessarily develop in consequence. Furthermore, it is unques* 
tionably a fact that anthracosis confers a relative immunity to pul- 
monary tuberculosis. The sharp, gritty particles of pulverized metal 
and stone are much more harmful, and lead not only to extensive 
interstitial fibrosis, but also predispose to tuberculous infection of 
the lungs, especially in the case of metal infiltrations. Oliver has 

drawn attention to the disas- 
trous inroads of Rand miners' 
phthisis among gold miners 
in the Transvaal who breathe 
air charged with quartz dust, 
and Robertshaw has empha- 
sized the high mortality of 
ganister miners' disease, or a 
form of phthisis secondary 
to pneumoconiosis affecting 
miners of ganister, a flinty 
mineral composed chiefly of 
silica. The dusts of wool, fur, 
hair, and other organic sub- 
stances are practically always 
contaminated by bacteria, 
and, therefore, are most likely 
to cause serious destructive 
processes, as well as inter- 
stitial fibrosis. Apart from 
their mechanical irritation, 
certain dusts also have a 
chemic action, and to this 
peril those engaged in the 
manufacture of paints, hats, and wall-paper are exposed, by being 
forced to breathe air full of dust charged with mercury, lead, or 
arsenic, as the case may be. 







Fig. no.— Pulmonary anthracosis (Jefferson 
Hospital Laboratories). 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 26 1 

No one's lungs are wholly free from dust, it is true, but ordinarily 
little or none of it reaches the pulmonary interstices, for the coarser 
particles are excluded by the cilia of the upper air-passages, while 
finer dust deposited in the trachea and bronchi is there incorporated 
with secretion or ingulfed by mucous and alveolar cells and subse- 
quently expelled by the action of the ciliated epithelium and by 
coughing and expectoration. But these protective measures, though 
adequate under ordinary circumstances, fail to prevent excessive 
deposits of finely granular inspirated material within the lungs of per- 
sons who day after day are compelled to inhale heavily dust-laden 
air. Under such conditions numerous dust-particles escape removal 
from the air-tubes, and, either naked or phagocyted, penetrate the 
mucosa, whence they enter the lymph-spaces and are carried 
by the lymphatics permanently to lodge in the intervesicular 
and bronchiolar tissues and in the thoracic lymphatic glands. 
Especially abundant are the particles deposited in the peribronchial 
and periarterial lymphatic nodules, in the tissues of the interlobular 
septa under the pleura, and in the substernal, tracheal, and bron- 
chial glands. Ordinarily, the granules go no farther than these 
adenoid structures, but exceptionally peribronchial glandular adhe- 
sions to the pulmonary veins open the door to the general circulation, 
with consequent pigmentation of the liver and spleen. 

In all probability visceral pigmentation is also due, at least to some 
extent, to the transference of ingested dust-particles from the alimen- 
tary tract to the blood-stream, via the lymphatics and the thoracic 
duct, and, furthermore, the same mechanism accounts for some of 
the pulmonary deposits, though to a distinctly minor degree. 

Although the pulmonary stroma can harbor an extraordinarily 
large amount of grit and other foreign particles for a long period 
without being damaged thereby, in time they irritate, provoke pro- 
liferation of the connective-tissue elements, and hence cause fibrous 
overgrowth. This process in the glands leads finally to their complete 
sclerosis, while the fibrous thickening of the intervesicular walls 
results in destruction of their blood-vessels and in obliteration of 
the air-vesicles, the affected tissues being thus deprived of air. As 
a rule, the cirrhosis begins in the peribronchial tissues, but ultimately 
it tends to invade other areas the fusion of which converts the lung 
into a more or less generally indurated mass; the infiltrations are 
likely to be most extensive and dense near the pulmonary apices. 
The lesions appear as scattered or diffuse patches of indurated, air- 
less tissue traversed by thickened, catarrhal bronchial passages, and 
surrounded by a zone of emphysematous lung. Their color varies 
with the character of the infiltrated material — jet black, grayish 



262 PHYSICAL DIAGNOSIS 

black, or slate color in the arthracotic lung; brick red or black in 
siderosis; and steel gray or unduly pale, perhaps with brown stains 
or stipples of altered blood-pigment, in chalicosis. Sometimes the 
fibroid territories become necrotic and cavernous (Charcot's ulceres 
du poumon) , and sometimes the cavities erode into a nearby bronchus, 
whereupon infection takes place, with rapid enlargement of, and sup- 
puration within, the excavation. Implication of the bronchial tree, 
in the form of chronic bronchitis with mural thickening, invariably 
attends the foregoing changes; emphysema generally develops in the 
course of time; in some instances there are bronchiectases; and a 
variable amount of pleural thickening and adhesion commonly 
ensues. The right side of the heart is enlarged as the result of the 
cirrhotic process, and not uncommonly the organ is dislocated by 
fibrous traction. 

Physical Signs. — The physical signs of pneumonoconiosis are those 
of chronic bronchitis, emphysema, and chronic fibroid induration 
of the lungs, associated in some instances with bronchiectasis and 
with chronic ulcerative phthisis. The sputum, which may contain 
tubercle bacilli, usually is abundant, and of mucopurulent, some- 
times fetid, character. It is blackened by coal-dust particles in 
anthracosis, reddened by bits of oxid of iron in siderosis, and 
shows fine silicate granules under the microscope in chalicosis. 

Diagnosis. — In a person whose occupation necessitates the in- 
halation of dust, a history of years of bronchitis and emphy- 
sema ultimately followed by progressive cirrhosis of the lung, together 
with the distinctive appearance of the sputum, is unmistakable 
evidence of pneumonoconiosis. Signs of pulmonary phthisis are 
also obvious in some cases, particularly in siderosis. 

PULMONARY ABSCESS (Purulent Pneumonia) 

Clinical Pathology. — Pulmonary abscess may arise in the various 
forms of aspiration pneumonia from infected particles sucked into 
the finer bronchi, wherein the contaminating material lodges and 
excites a suppuration which extends to the contiguous vesicular struc- 
tures. Occasionally, croupous pneumonia terminates in suppuration 
of the lung, and, less commonly, this serious accident follows ordinary 
catarrhal pneumonia. Abscess of the lung due to the extension 
of some primary focus of infection, either by contiguity or by the 
lymphatics, is a potential complication in phthisis, pneumonoconiosis, 
bronchiectasis, empyema, mediastinal abscess, esophageal cancer, 
hepatic abscess, and suppurating hydatid cyst of the lung or the 
liver. Stab wounds of the Chest-wall, or even a presumably sterile 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 263 

paracentesis, may carry pyogenic infection to the pulmonary 
tissue. In pyemic conditions the origin of pus foci in the lungs 
is traceable to emboli laden with pus-germs lodged in the termi- 
nal branches of the pulmonary artery. 

Pulmonary suppuration may take the form of a solitary abscess 
of variable size, of multiple abscesses usually of small size, or of 
diffuse purulent infiltration. If of moderate extent, the purulent 
area sometimes is walled off from the surrounding lung by an imperme- 
able fibrous capsule, but, on the other hand, practically an entire 
lobe may be invaded by a huge solitary abscess, developing either 
by the progressive spread of the primary focus or by the coalescence 
of several small points of pus. An abscess of the lung begins as an 
intense suppurative pneumonitis followed by softening, necrosis, 
and sloughing of the infected pulmonary tissue which, in consequence, 
undergoes excavation. The wall of the cavity, inclosing a collection 
of pus and disintegrated pulmonary tissue, is lined at first with ragged 
remnants of the necrotic lung and with inflammatory tissue, but 
later this lining ordinarily is replaced by a smooth pyogenic mem- 
brane, the contiguous lung being consolidated by infiltration and by 
a variable degree of fibrosis. Outside this none too firm a barrier 
the lung is more or less engorged, edematous, and hemorrhagic. 
Apart from the possibility of being isolated by encapsulation, a small 
abscess may ultimately heal by absorption of the purulent matter 
and by cicatrization, but, on the contrary, the infection may spread 
to other parts of the lung. Drainage is sometimes established by 
erosion into a bronchus; or the pus may invade the pleural cavity 
and cause empyema. Infected emboli giving rise to small, usu- 
ally numerous, wedges of pus lying base toward and close to the 
pleura, are an especially common factor of this accident. It should 
be added that empyema is also attributable to infection through 
pleural membranes permeable by bacteria, but intact in the sense 
that no actual breach exists therein. Exceptionally, a channel is 
worn, via an abscess cavity, between a bronchial tube and the pleura, 
and under this circumstance pyopneumothorax almost inevitably 
supervenes. Pus diffused through the interstices of the lung, without 
the formation of circumscribed abscess, is accounted for by dissemi- 
nation of pyogenic microorganisms by the lymph-stream. 

Physical Signs. — Abscess of the lung affords definite thoracic 
signs only when it is of comparatively large size and superficial situa- 
tion, in which event the objective signs of pulmonary consolidation 
and excavation are appreciable, together with corroborative evidence 
such as dyspnea, cough, "pump-handle" pyrexia, sweats, and emaci- 
ation. Signs of bronchitis and of pleurisy, both frequent concomitant 



264 PHYSICAL DIAGNOSIS 

lesions, are commonly demonstrable, and in certain cases it is not 
difficult to find some primary affection, either within or remote 
from the lungs, to explain the pulmonary suppuration. The sputum 
is generally profuse, has a nauseatingly sweet and heavy odor, is of 
purulent character, and may contain, in addition to pus-cells and 
bacteria, shreds of elastic fiber and necrotic tissue from the lung. 
Copious gushes of expectoration sometimes occur when the secretion 
rising within an abscess cavity overflows into the bronchial outlet 
and in so doing provokes a fit of so-called "evacuative cough." 
When the suppurative process is composed of multiple small foci or 
is diffusely infiltrated, no clear physical signs can be looked for, and 
under these circumstances the symptoms of septic intoxication rule 
the clinical picture. 

Diagnosis. — The character of the sputum, a clinical picture of 
septic poisoning, and physical signs of pulmonary softening and 
excavation appearing as a sequel to a primary lesion of the lung are 
the cardinal points of diagnosis. Empyema may be attended by 
constitutional symptoms like those of pulmonary abscess, and, should 
the purulent matter be discharged through a bronchus', the patient 
may suddenly cough up mouthfuls of pus, either practically pure or, 
rarely, fetid, but quite free from elements derived from disintegration 
of the lung. This fact, with the discovery of fluid in the pleura, shows 
the pleural origin of the pus. Abscess versus gangrene of the lung 
is referred to under the latter affection. (See p. 267.) 

PULMONARY GANGRENE (Necropneumonia; Pulmonary Sphacela- 
tion or Mortification) 

Clinical Pathology. — A dual factor is at work in producing 
gangrene of the lung: diminished vitality of the pulmonary tissue and 
infection of the devitalized part, the former being due to inadequate 
blood-supply and the latter to the invasion of pyogenic and associated 
bacteria. Subnormal tissue resistance must be regarded as the 
essential predisposing cause of gangrene, and this serves to explain 
the relative frequency of this grave affection in persons whose nutri- 
tion and defensive powers have been lowered by diabetes, alcoholism, 
chronic debility, and exhausting fevers, and its rarity in those whose 
health has not been undermined. Bacterial infection of vascularized 
pulmonary tissue generally means nothing more than abscess, at 
least primarily, but when the tissue's blood-supply is cut off, infec- 
tion induces mortification. Important causes of pulmonary gangrene 
include aspiration and croupous pneumonias, abscess, cancer, and 
tuberculosis of the lung, bronchiectasis, and bronchial stenosis by 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 



265 



foreign body or by pressure of an aneurism or neoplasm, and con- 
tamination by some extrapulmonary necrotic process. Pulmonary 
embolism, particularly when septic, is likely to set up tissue death in 
the infarcted area beyond the clot, and this factor explains the occa- 
sional development of pulmonary gangrene in abscess of the middle 
ear, the mastoid, or the brain, in ulcerative endocarditis, in femoral 
thrombosis, and in acute febrile infections. Less commonly, sterile 
emboli account for a gangrenous lung. 

Pathologically, there are two well-defined types of pulmonary 
gangrene: the circumscribed and the diffuse. Circumscribed gan- 
grene may consist either of a single area or of multiple foci of dead 
pulmonary tissue of red dish -brown, greenish, or black appearance, 
and sharply delimited from the neighboring inflamed lung (Fig. in). 
As the tissue disintegra- 
tion and solution proceed, 
the gangrenous patch 
softens and is converted 
into an excavation with 
rough, shaggy walls in- 
closing a fetid semifluid 
mass of necrotic debris. 
Bronchi near or within 
such a cavity are fre- 
quently eroded, and in 
consequence furnish an 
outlet for the putrescent 
material, and arteries 
traversing a gangrenous 
area become thrombotic 
and perhaps so worn that 
free hemorrhage takes 
place. The pulmonary 
tissue around a circum- 
scribed gangrenous lesion 
is extremely hyperemic, 
and more or less solidified by infiltration and by edema. As in abscess 
of the lung, a subpleural spot of gangrene excites pleural inflamma- 
tion, thickening, and adhesion, and if the membranes be perforated, 
empyema, sometimes pyopneumothorax, supervenes. Intense bron- 
chitis, generally of the putrid type, and inflammatory swelling 
of the bronchia] glands are common complications of pulmonary 
gangrene. Aspirated particles of fetid bronchial secretion may excite 
gangrenous bronchopneumonia in either the affected or the opposite 




-Gangrene of the lung (Jefferson Hos- 
pital Laboratories). 



266 PHYSICAL DIAGNOSIS 

lung. In some instances the mediastinum, the pericardium, or the 
abdomen is contaminated by the process of erosion, and embolic 
transference of the infection is not unlikely to occur, producing lesions 
of distant organs, for example, abscess of the brain. Diffuse gangrene 
of the lung, lacking the sharp line of demarcation so distinctive of 
the circumscribed form, sometimes arises by extension of the latter, 
or it may be a primary diffuse process consequent to pneumonia, 
bronchiectasis, putrid bronchitis, or pulmonary artery thrombosis. 
The greater part, if not the whole, of a lobe is transformed into a 
black or greenish mass of putrid necrosis, farthest advanced in the 
center of the lesion, whence the destructive changes gradually blend 
with those of the surrounding inflamed and consolidated lung. The 
diseased tissue at first is of firm, solid consistence, but later it becomes 
soft, pultaceous, and riddled with communicating cavities of various 
size. Fatal septicemia, septic thrombosis, hemorrhage, or pyopneu- 
mothorax is the sequel to be expected in this type of pulmonary 
gangrene. 

Physical Signs. — Little can be learned from examination of the 
lungs unless the gangrenous area be extensive and near the surface, 
when, like abscess, it produces the physical signs of pulmonary 
solidification, softening, and excavation. Furthermore, it is almost 
invariably the rule also to find evidences of intense bronchial inflam- 
mation, pleurisy, and other attendant lesions either provocative of, 
or consequent to, the rotting lung. When a gangrenous area com- 
municates with a bronchus, the patient's breath becomes horribly 
fetid and the sputum abundant, thin, and usually of a dirty greenish- 
brown hue. The sputum, too, smells vilely, for it reeks with decom- 
posed tissue, pus, and putrefactive bacteria. On standing, it tends 
to separate into three layers: a dark granular sediment, a middle 
zone of thin liquid, and a top layer of mucopus. Microscopically, 
aside from shreds of necrotic pulmonary tissue and perhaps elastic 
fibers, the sputum ordinarily shows pus and red blood-cells, blood- 
pigment, Dittrich's plugs, fat-globules and fatty acid crystals, choles- 
terin, leucin and tyrosin, swarms of bacteria, and, exceptionally, 
flagellate organisms and sarcinae. 

Diagnosis. — The fetor of the breath and the character of the 
sputum are the two most distinctive features of pulmonary gangrene, 
which in typical instances is also attended by physical signs of pul- 
monary disintegration, by moderate fever and rapid pulse, by dyspnea, 
cough, and sometimes hemoptysis, by emaciation and prostration, 
and, in certain cases, by delirium. When the subject gives a history 
of diabetes or other debilitating disease and has suffered from some 
acute pulmonary lesion prior to the onset of this pertinent symptom 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 267 

group, the diagnosis is reasonably certain. On the other hand, not 
infrequently the diagnosis of gangrenous lung must be made more by 
inference than by clinical proof, for in some instances there is neither 
foul breath nor necrotic sputum; in others these two diagnostic 
mainstays are referable to some non-gangrenous lesions; and in still 
others there are indefinite chest signs, or none at all. Thus, in the 
condition termed latent pulmonary gangrene, met with particularly 
in diabetics and in the insane, the patient's breath is untainted and 
the sputum odorless and mucoid, probably because the lung necrosis, 
though sometimes extensive, progresses leisurely, is well circumscribed, 
and does not open into a bronchus. In a case of this sort, affording 
possibly nothing but a suspicious history and signs of consolidation, 
an antemortem diagnosis of gangrene is not possible. Stinking 
breath and fetid expectoration may arise from purulent, decomposing 
lesions of the bronchi, lungs, and pleural cavity, without the coexist- 
ence of gangrene. 

In pulmonary abscess the breath is foul, but the odor is distinctively 
sweetish and not so fetid and heavy and penetrating as in gangrene; 
while the sputum, frequently coughed up in copious gushes, consists 
chiefly of pus, though it occasionally contains shreds of disintegrated 
lung. 

In putrid bronchitis the breath is horribly fetid — only theoretically 
less so than in gangrene — but the foul sputum, abundant and sero- 
purulent, does not contain pulmonary shreds nor elastic fibers. 

Bronchiectasis taints the subject's breath with an odor of putre- 
faction only a shade less offensive and permeating than gangrene. 
This is true, notably, of saccular bronchiectases characterized by 
the periodic discharge of large quantities of sputum charged with 
putrescent matter and pus, but generally free from elastic fibers, 
save in the event of bronchial ulceration. 

Advanced pulmonary tuberculosis , with cavities full of decomposing 
secretion, may be responsible for fetid breath and for foul sputum 
containing elastic fibers, but the breath, despite its disagreeable 
odor, has not the vile smell of gangrene, the sputum is filled with 
tubercle bacilli, and the patient usually shows unmistakable signs 
of apical excavation and of systemic inroads by the infection. 

Bad breath incident to ozena and to alveolar necrosis obviously 
can be identified by examination of the nose and the mouth. 

PULMONARY NEOPLASMS 
Carcinoma. — Carcinoma, the most frequent type of pulmonary 
neoplasm, is rarely of primary origin, for the lung is usually invaded 
by the transference of a neoplastic process from an adjacent or a 



2 68 



PHYSICAL DIAGNOSIS 



distant initial lesion. In Stevens's analysis of more than 32,000 
autopsies by various foreign reporters only 43 cases of primary 
pulmonary cancer are recorded. The tumor, commonly an 
encephaloid, may be situated in a neighboring structure, such 
as the pleura, esophagus, breast, or mediastinum, or in some 
remote part, like the liver, gastro-intestinal canal, or uterus, 
whence bits of the original tumor are carried, by the lymph 
or blood, to the lung, therein to lodge, proliferate, and replace 
the pulmonary tissue. A lung may also be attacked by a can- 
cer originating in the mucous glands of the bronchi or possibly 
in the alveolar epithelium and eventually spreading through 




Fig. 112.— Radiograph of- a pulmonary neoplasm. Anterior aspect, showing shadow 
of growth in left lung. (Plate by Dr. W. F. Manges.) 

both lungs. Bilateral implication is the rule in growths of secondary 
type, and in primary cancer the tumor may either be confined to 
the lung originally affected, or spread to the other lung and to nearby 
structures. Primary carcinoma of the lung is decidedly more fre- 
quent in men than in women, and the lesion in many instances 
appears to be directly attributable to trauma; cobalt miners are 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 269 

supposed to be exceedingly predisposed. Of the two sexes, women 
are the more susceptible to secondary cancer. 

Malignant growths of the lung primarily cripple the organ's res- 
piratory function by replacing the normal pulmonary tissue, and 
subsequently, as the neoplastic consolidation progresses, necrotic 
changes are prone to supervene both in the malignant areas and in 
other parts of the lung. In an extreme instance virtually an entire 
lung is invaded by the new-growth, ordinarily by the coalescence 
of numerous foci multiplying by local metastases from the parent 
lesion, but exceptionally arising by a more diffuse extension, radially 
or eccentrically, from the original deposit. In the immediate vicinity 
of the neoplastic areas the lung is collapsed, carnified, and edematous, 
and in other parts the vesicles are compensatorily dilated. When a 
malignant mass impinges closely against a bronchus, atelectasis and 
its unfortunate consequences arise in the corresponding vesicular 
territory; when a bronchus is perforated, bits of tumor tissue may 
enter the tube, to be coughed up and expectorated, or to be aspirated 
into other bronchial twigs, therein exciting bronchopneumonic proc- 
esses and also secondary foci of the original tumor. Malignant 
areas communicating with a bronchial tube are most susceptible to 
bacterial infection, and hence to gangrenous degeneration and excava- 
tion, while the same thing may happen to patches of consolidated 
inflamed lung similarly situated. The growth may compress the 
gullet, the superior vena cava, the internal mammary artery, or the 
pulmonary vessels, giving rise to pressure symptoms similar to those 
found in mediastinal tumor. Pleural inflammation, setting up adhe- 
sions and thickening or attended by effusion, often of hemorrhagic 
character, is inevitable when the malignancy reaches the surface of 
the lung. In the rare event of pleural perforation pneumothorax, 
of course, ensues. With the extension of the malignant process 
beyond the confines of the lung, invasion of the" tracheobronchial, 
mediastinal and cervical glands, the pleural membranes, and the 
opposite lung is the natural sequence. 

The physical signs of pulmonary carcinoma naturally are subject 
to wide variance in the individual case, according to the site and 
size of the neoplastic infiltration and the bronchopulmonary damage 
thereby caused. Cachexia, though more or less apparent, tends 
to develop more slowly and less conspicuously in cancer of the lung 
than in cancer elsewhere situated. The superficial veins of the neck 
and thoracic wall may be distended abnormally in consequence 
of pressure upon the superior cava and internal mammary vein. 
The respiratory mobility of the affected side is sometimes restricted 
and the contour of the chest altered, being bulged and intercostally 



270 



PHYSICAL DIAGNOSIS 



widened by a massive growth, and retracted by one attended by dense 
fibrosis and adhesions or by pressure atelectasis. Vocal fremitus 
is very variable, being determined chiefly by the conducting properties 
of the neoplasm and the state of the surrounding vesicular structure. 
Dulness is afforded by a large, diffuse, superficial tumor; hyperreso- 
nance or tympany, by a cancerous excavation within range of the 
percussion strokes; and wooden flatness, by extensive pleural implica- 
tion. Abnormalities of the respiratory murmur include suppressed 
breathing, due to a moderately disseminated growth; loud tubular 
respiration, produced by a large compact infiltration; and the amphoric 
tone of a cavity. Various rales, of bronchial, vesicular, and pleural 




Sarcoma of the lung (Jefferson Hospital Laboratories). 



origin, are audible when there is coexistent bronchitis, congestion, 
edema, or pleurisy. 

Sarcoma. — As a pulmonary growth sarcoma is distinctly less com- 
mon than carcinoma, and, save in exceptional instances, is of second- 
ary development, the initial tumor, according to West, existing in 
bone in one- third of all cases. Hypernephroma is followed by 
pulmonary metastasis of sarcomatous type in fully 60 per cent. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 27 1 

of cases (Wooley). As a rule, the growth is disseminated through 
both lungs. Pulmonary sarcoma is peculiar in two details: the 
long interval that may elapse in secondary cases between the ap- 
pearance of the initial tumor and its metastasis in the lung, and 
its frequency in advanced life rather than in youth. A primary 
sarcoma of the lung, which usually is unilateral, is a very rare lesion, 
and commonly consists of an endothelioma originating in the pleura, 
or, exceptionally, in the lymph-follicles or blood-vessels. 

The physical signs of pulmonary sarcoma do not differ from those 
of the other type of malignant disease of the lung discussed above, 
and, therefore, need not be further discussed. 

ACTINOMYCOSIS 

Pulmonary actinomycosis, though rare, is of clinical interest 
because of its more or less close resemblance to certain other 
pulmonary diseases, notably tuberculosis. The ray-fungus may 
invade the lung primarily, or may extend thereto by metastasis, 
by bronchogenic infection from a buccal lesion, or by direct 
extension from a neighboring focus. The process is essentially 
chronic, progressively destructive, and most unlikely to become 
arrested. Ordinarily, it is characterized by chronic diffuse bronchitis, 
attended by fetid mucopurulent sputum charged with actinomycelic 
granules. In such instances bronchopneumonic lesions some- 
times develop, from the inhalation of contaminated matter, and set 
up a so-called miliary type of the disease, resembling in its general 
features miliary tuberculosis. The growth of fungous nodules 
in the lungs leads ultimately to obliteration of the vesicular structures 
and induces a condition of exudative catarrhal pneumonia; suppura- 
tion, softening, and excavation of the actinomycotic area occur; 
and in some cases perinodular fibrosis develops, which not only has 
a tendency to encapsulate the specific lesions, but also to spread 
through the adjacent interalveolar tissues. Thus, the greater part 
of an actinomycotic lobe may be converted into a dense fibrous mass, 
riddled with pus-cavities, traversed by fistulous tracts; and stippled 
with less mature foci in different phases of development. Extension 
of the process toward the pleura produces inflammation and adhesion 
thereof, and, in the course of time, after the invasion of these mem- 
branes, the chest-wall may become implicated or the abdominal 
cavity penetrated. 

The physical signs of pulmonary actinomycosis are in no sense 
distinctive, for usually they resemble those of a stubborn catarrhal 
bronchitis, of a chronic bronchopneumonia with softening and excava- 
tion, or of an abscess of the lung. Phthisis in its various phases is 



272 PHYSICAL DIAGNOSIS 

most often counterfeited, sometimes with surprising fidelity, by the 
general clinical picture, but in such a contingency the true nature 
of the symptoms is surely revealed by examination of the sputum. 
This contains the characteristic actinomyces granules (" sulphur 
granules"), consisting of minute yellow-brown or gray grains, which, 
when crushed, are found to be made up of an obscure central gran- 
ular mass, from which radiate straight and undulating threads of 
mycelia, many showing club-like swellings. 

ECHINOCOCCUS CYST 

The lung or the pleura, particularly the former, is affected in 
about 8 per cent, of all cases of echinococciasis, the lesion com- 
monly being secondary to an hepatic hydatid which has ruptured 
through the diaphragm or, exceptionally, reached the lung by way 
of the hepatic vein, inferior cava, and right heart. The development 
of a single cyst in one lung is more frequent than the growth of mul- 
tiple cysts, either unilaterally or bilaterally, and in most cases the 
lower right lobe is the seat of the lesion. As the size of the cyst or 
cysts increases, corresponding compression of the lung is provoked, 
and the tumor may dislocate the mediastinal structures, encroach 
upon the pleural sac, and depress the diaphragm. Death of the 
cyst is likely to induce inflammatory changes resulting in suppura- 
tion, gangrene, and cavity formation; or the cyst fluid may become 
absorbed and inspissated, the wall atrophy, and the process undergo 
encapsulation by lime salts. So long as a hydatid lives and grows 
and remains of moderate size, neither irritation nor inflammation 
of the lung is likely to supervene. Should a cyst rupture, it generally 
does so into a bronchus, whereupon purulent material,, bits of cyst 
membrane, hooklets, and free blood may be expectorated; less 
commonly it bursts into the pleura, causing pyopneumothorax; and 
exceptionally it suppurates through the chest-wall. 

Physical signs are not demonstrable until the cyst attains consider- 
able size, excites inflammatory changes, or ruptures. Suggestive, 
but not distinctive, signs include cough, dyspnea, hemoptysis, local 
bulging, restricted breathing, and a circumscribed dull area over 
which vocal fremitus, vocal resonance, and respiratory sounds are 
impaired or abolished. The heart and the liver may be displaced, 
and not uncommonly there are evidences of bronchitis, pulmonary 
consolidation, and pleural effusion. Over a large superficial cyst 
it is sometimes possible to detect hydatid fremitus and sonorous 
hydatid resonance (q. v.). Eosinophilia is an important sign of 
early, active echinococciasis. Exploratory puncture may give the 
correct clue to a puzzling group of physical signs, and the sputum 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 273- 

sometimes affords pathognomonic findings, such as hooklets and 
laminated membrane. (See p. 60.) 

PLEURISY (Pieuritis) 

The term pleurisy is applicable to numerous types of acute and 
chronic pleural inflammation that differ greatly in extent, intensity, 
and character, according to the circumstances prevailing in the 
individual instance. The lesion may be confined to a circumscribed 
area, or implicate the greater part of the pleural surfaces; its pre- 
dominant character is fibrinous, serofibrinous, or purulent; and its 
origin is more frequently secondary and symptomatic than pri- 
mary or idiopathic. For clinical study it is convenient to recognize 
the following main types of pleural inflammation, although, patho- 
logically, such clear-cut distinctions are not always warranted: 
(a) Acute -fibrinous pleurisy, (b) Serofibrinous pleurisy, (c) Puru- 
lent pleurisy, (d) Circumscribed pleurisy, (e) Chronic adhesive 
pleurisy. 

By far the greatest number of cases of pleurisy are of the secondary 
or symptomatic type, arising most commonly from the extension of 
inflammatory diseases of the lungs and adjacent parts, of which 
lesions tuberculosis is of especial importance. Rarely does the 
pleura escape damage in this disease, though not always does it 
become actually tuberculous; less frequently a pulmonary tuber- 
culosis is lighted up by a primary tuberculous focus of the pleura. 
To the group of pulmonary factors of pleurisy also belong pneumonia, 
infarction, abscess, gangrene, and neoplasm; while in other cases the 
process may arise by extension in consequence of disease of the 
pericardium, the peritoneum, the liver, or the bony thorax. Many 
pleurisies are traceable to such underlying conditions as rheumatic 
fever, nephritis, gout, syphilis, and alcoholism. 

Of primary pleurisy, a comparatively rare condition, there is little 
to be said. A small minority of cases correspond to this caption — 
for example, those developing in a subject of low vital resistance 
after exposure to cold and dampness; but many apparently primary 
pleurisies are, in reality, of the secondary type, though the under- 
lying factor may be masked. Bacteriologically, the tubercle bacillus, 
the pneumococcus, and the streptococcus are the three bacteria 
principally concerned as the causes of various forms of pleurisy, 
and of these organisms the first is the most frequent offender, the 
second the least harmful, and the last the most virulent. Less com- 
monly pleurisy is referable to other microorganisms, notably to 
staphylococci, pneumobacilli, colon bacilli, typhoid bacilli, and diph- 
theria bacilli. 
18 



274 PHYSICAL DIAGNOSIS 

ACUTE FIBRINOUS PLEURISY (Acute Dry or Plastic Pleurisy? Pleuritif 

Sicca) 

Clinical Pathology. — This form of pleurisy, which is more often 
confined to one or several circumscribed areas than generally dis- 
seminated, is accompanied by little or no accumulation of serum, 
the inflamed membranes, after a primary stage of acute injection, 
being coated with a scanty fibrinous exudate which obscures the 
normal glistening surface of the pleura and renders it dull, opaque, 
and lusterless. In a moderate inflammation with trifling prolifer- 
ation of fibrous tissue, the exudate may soon undergo fatty degen- 
eration and partial absorption, leaving merely small pearly patches 
of pleural thickening to mark the site of the lesion. If the inflam- 
mation be more active, however, the inflamed parts are covered by 
an abundant, thick lymph deposit, tending rapidly to become organ- 
ized and thus ultimately to agglutinate the opposed pleural surfaces 
into a permanent fibrous union. 

Physical Signs. — Inspection. — In order to ease the pain the 
patient, when erect, instinctively lowers the shoulder and relaxes 
the musculature on the affected side, and lies thereupon when 
confined to bed. The respiratory movements are shallow and 
the diaphragm shadow is obscured, especially on the pleuritic 
side; the breaths come and go in an uncertain, jerky, and painful 
manner; and the subject suffers from persistent, dry, and restrained 
cough. These objective symptoms of pleuritic pain are by no means 
constant, for, remarkable as it may seem, the patient, despite wide- 
spread pleural inflammation, may complain of no discomfort what- 
ever. Dilatation of the pupil on the affected side, from sympathetic 
nerve irritation, is a finding of some suggestiveness. 

Palpation and percussion are usually negative, save in the event of 
an abundant, thick exudate which may enfeeble vocal fremitus, 
modify the percussion resonance, and increase the tactile resistance 
of the area percussed. Distinct friction fremitus is sometimes pal- 
pable over the inflamed pleural surfaces. 

Auscultation. — Friction-sounds are audible over the site of the 
lesion during the first few days of the disease, after which they dis- 
appear as the pleuritis subsides, usually with a more or less per- 
manent adhesion of the inflamed pleural surfaces. In this type of 
acute pleurisy the friction, usually most distinct during inspiration, 
resembles a series of delicate, crepitating, jerky sounds, which, apart 
from their dry, superficial character, are very like the vesicular crepita- 
tion. The ordinary auscultatory site of pleural friction is shown by 
Fig. 90, p. 171. Pieuropericardial friction sounds, generated by 
the cardiac impact, are audible when the pleural surfaces adjacent 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 275 

to the pericardium are roughened. (See p. 172.) The vesicular 
murmur, though frequently suppressed, shows no definite pathologic 
modification, and vocal resonance remains of normal degree. 

Diagnosis. — The characteristic friction-sound is sufficient for 
the direct diagnosis of acute plastic pleurisy, irrespective of the 
patient's cough, respiratory distress, fever, and other objective symp- 
toms. Routine chest examinations in subjects of various pulmonary 
disorders will reveal a surprisingly large number of unsuspected pleuri- 
sies, whose existence has provoked neither pain nor any other dis- 
comfort. It was doubtless the acute type of dry pleurisy that the 
great Dutchman, Boerhaave, had in mind when, more than two 
centuries ago, he spoke of "a sharp pricking inflammatory pain in 
the side, greatly increased in the act of inspiration, but abated in 
expiration, or by holding the breath," and when he referred to "a 
cough, which is almost incessant, and which, exciting great pain, 
is, therefore, stifled or suppressed by the patient." 

Having discovered a pleural inflammation, it is important to decide, 
by further inquiry, if the lesion be uncomplicated, if it be sympto- 
matic of some diathetic state, or if it be secondary to pulmonary 
pericardial, hepatic, or peritoneal lesion. 

Both intercostal neuralgia and pleurodynia, in so far as pain is 
concerned, may closely simulate dry pleurisy, but in neither of these 
conditions is there friction or fever. Intercostal neuralgia is most 
commonly found in women who suffer from other nerve pains and 
are of the neurotic temperament, and the pain, which is lancinating 
and aggravated by motion, radiates along the course of the superficial 
branches of the intercostal nerves, whose points of exit (in the para- 
sternal and axillary lines and at the bend of the ribs) are the seat 
of the most exquisite pain on palpation. 

Pleurodynial pain, which is prone to occur in connection with 
other myalgic symptoms, is also intensified by motion, but it can be 
circumscribed to the intercostal muscles by making pressure over 
the interspaces. In the exceptional case subphrenic peritonitis {q. v.) 
is the source of friction-sounds audible over the lower part of the 
thorax. 

SEROFIBRINOUS PLEURISY (Pleurisy with Effusion) 

Clinical Pathology. — In serofibrinous pleurisy the primary 
changes are essentially those of the fibrinous type of the disease, 
except that they are usually more acute and more widely distributed; 
as a rule, they are unilateral. The affected surfaces are coated with 
a fibrinous exudate which, in some instances, consists merely of 
a thin, smooth, pale film, and in others of a thick, buttery deposit 



276 PHYSICAL DIAGNOSIS 

of shaggy, ragged, honey-combed appearance. Attending these 
primary changes there is a free outpouring of inflammatory exudate, 
which gravitates to the lowest part of the pleural sac, save when, 
owing to the existence of pleural adhesions, it is hemmed in at a 
higher level. The amount of exudate poured out varies within the 
widest limits in different cases: ordinarily it ranges approximately 
between 16 and 64 ounces (480 and 1920 mils), but exceptionally it 
is decidedly larger — 100 ounces (3000 mils) or more, or, as in Lie- 
bermeister's unique case, 245 ounces, i. e., 7350 mils. The exudate is 
composed of a coagulable albuminous fluid containing fibrin, blood- 
cells, swollen endothelial cells, uric acid, cholesterin, and sugar. 
These, as well as the other constituents of the exudate, have been de- 
scribed in a preceding section. (See p. 53.) If the fibrin content be 
moderate, the fluid is of a clear straw color and contains white fib- 
rinous flocculi; if the fibrin be excessive, the exudate becomes turbid 
and is filled with numerous matted, curd-like masses of fibrin which 
tend to adhere to the pleural surfaces in thick, creamy layers. 

The term hemorrhagic pleurisy is used when the exudate con- 
tains sufficient erythrocytes obviously to tinge it pink, red, or brown, 
such a change not becoming appreciable until the erythrocytes 
number at least 6000 to the cubic millimeter of fluid (Dieulafoy). 
Blood-stained effusions are very suggestive of tuberculosis and of 
cancer; less commonly they attend cardiac, renal, and hepatic lesions, 
the specific febrile infections, the several hemorrhagic diatheses, and 
various low asthenic states; and exceptionally they result from simple, 
though most intense, pleuritis. Hemorrhagic pleurisy is sometimes 
referable to the rupture of a vessel coursing through a false membrane 
organized upon the site of a recurrent pleural inflammation. True 
hemorrhagic pleurisy must be distinguished from an ordinary sero- 
fibrinous effusion accidentally tinged with blood by a tear in the lung 
made by an aspirating needle, and from the accumulation of pure 
blood in the pleural sac, or hemothorax (q. v.). 

So-called chyliform pleurisy, distinguished by a turbid exudate 
of milky appearance, is met with in exceptional cases of both sero- 
fibrinous and purulent effusions, as the result of extensive fatty changes 
in the cellular elements of the exudate, which, microscopically, shows 
many fat-globules, fatty leukocytes and endothelium, and cholesterin 
crystals. Effusions of this type (hydrops adiposus), which are likely 
to be of tuberculous origin, of a primarily purulent nature, and of 
chronic duration, are to be distinguished from genuine chylothorax 
(hydrops chylosus), or the presence of pure chyle within the pleural 
sac (q. v.). 

If the exudate be of considerable volume, the lower part of the 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 277 

overlying lung is compressed, collapsed, and perhaps deprived of air 
and blood, while the pulmonary tissue above this zone of carnifica- 
tion is vicariously overdistended; in a very large and persistent effusion 
the pulmonary carnification may attain so extreme a degree that 
subsequent restoration of the lung is impossible. The mediastinum 
is dislocated toward the sound side, and the heart undergoes a similar 
displacement. The apex, though shifted, is never rotated (Osier), 
and its normal relative position to the base is not altered. The 
weight of a large effusion causes the diaphragm to sag abnormally 
low and restricts its respiratory excursions ; if right-sided, the effusion 
depresses the liver, and if left-sided, the stomach, the transverse 
colon, and the spleen. In some instances the vascular trunks within 
the thorax are considerably pressed upon by the exudate. After the 
removal of the exudate, whether by absorption or by aspiration, there 
is a certain amount of connective-tissue formation at the site of the 
lesion, in favorable cases amounting to little more than a grayish 
area of moderate thickening or to limited adhesions of the opposed 
pleural surfaces. 

The factors of serofibrinous pleurisy are virtually those of the 
fibrinous form, and, therefore, do not call for further mention. The 
importance of tuberculosis as an exciting cause, however, must be 
especially emphasized, for a large proportion of cases are tuber- 
culous, either primarily or in consequence of infection from foci 
in the lungs, peritoneum, or other parts of the body. 

Physical Signs. — Inspection. — The sharp pain of the preexudative 
stage excites both hurried and restricted breathing, which later, as 
the inflamed, sensitive pleural surfaces are bathed in the exudate, 
gives way to painless dyspnea, the urgency of which is related chiefly 
to the extent of the effusion; should there be patches of dry pleurisy 
elsewhere, however, painful respiration persists despite the effusion. 

An extensive effusion causes moderate distention and decided 
immobility of the affected side, but comparative measurements of 
the two halves of the thorax will show that this increase of volume 
is actually much less than it appears, since it rarely amounts to more 
than 1 or 1^ inches (2.5 to 3.75 cm.). The lower intercostal spaces are 
unduly shallow or even quite effaced, so that the contour of the lower 
chest is smooth and rounded. In some patients the interspaces are 
wider than normal, but in young children they may be distinctly 
narrowed, by reflex contraction of the intercostal muscles — a sign 
described by Przewelski. The respiratory excursions of the affected 
side are considerably restricted and the diaphragm shadow of Litten 
is correspondingly abolished, while the opposite half of the thorax 
shows exaggerated expansion, as a matter of compensation. Inspec- 



278 



PHYSICAL DIAGNOSIS 



tion of the back may reveal a deviation of the spine toward the side 
of the effusion. 

The cardiac impulse is dislocated upward and toward the unaffected 
side. In a left-sided effusion it may be visible in the epigastrium 
or to the right of the sternum, sometimes as far outward as the neigh- 
borhood of the right midclavicular line and as high as the fourth or 
the third interspace; should the apex be pushed directly behind the 
sternum, no impulse will, of course, be visible. In a right-sided 




Radiograph of a left pleural effusion. (Plate by Dr. W. F. Manges.) 



effusion the apex-beat may be displaced an interspace upward and 
carried outward to or even beyond the left midclavicular line. C. L. 
Greene has pointed out that the cardiac impulse approaches the 
median line with deep inspiration, and recedes therefrom with expira- 
tion, this sign being especially apparent in effusions of moderate size. 
It is demonstrable in some cases on ordinary inspection, but is more 
clearly recognized with the fluoroscope. 

Fluoroscopic examination shows a shadow over the site of the 
effusion, and also indefiniteness of the costal and diaphragmatic 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 279 

outlines, with abnormal depression and limited mobility of the 
latter. The lung above the effusion, if unduly dense, casts a 
correspondingly dark shadow, and the heart encroaches upon the 
unaffected side. The shadows cast by serofibrinous and by purulent 
effusions do not differ in density, according to Williams. 

Palpation. — In the dry stage of the inflammation the voice-sounds 
are unaltered, but occasionally a friction fremitus is appreciable 
on palpation. Enfeeblement or total abolition of vocal fremitus 
is most convincing evidence of a collection of fluid within the pleura, 
but, unfortunately, this sign is not invariably obtainable, owing to 
the coexistence of factors whereby tactile fremitus is exaggerated. 
Thus, despite the presence of a well-marked effusion, the voice vibra- 
tions may be transmitted through the liquid by bands of adhesions 
or by a bronchus dislocated against the chest-wall, while in other 
instances they may travel, via an overresilient parietes, from the sound 
to the affected side. It is in children especially that persistence of 
vocal fremitus is not to be regarded as incompatible with a pleural 
effusion. The fremitus is exaggerated over the site of the compressed 
lung above the effusion. Normal vocal fremitus reappears as the 
effusion diminishes in volume, except over areas where the thickening 
of the pleura is sufficient to damp the vibrations of the spoken voice. 

Aside from showing the intensity of the vocal fremitus, palpation 
is useful in determining differences in the contour and the expansion 
of the two halves of the chest, in locating the cardiac impulse, and 
in ascertaining the level of the lower border of the liver. Reflex 
muscular contraction and rigidity below the twelfth rib on the 
pleuritic side is commonly appreciable (Ramond). 

Percussion. — As an exudate accumulates within a pleural sac the 
percussion sound below the upper level of the liquid first becomes 
impaired, then frankly dull, and finally flat, as the fluid replaces 
pulmonary tissue. These auditory percussion signs are attended 
by a sense of increased resistance to the pleximeter finger, corre- 
sponding to the degree of airlessness of the area percussed, and in 
the typical case becoming so extreme that the finger perceives no 
trace of the normal parietal resiliency; under such circumstances 
the flatness acquires a high-pitched, wooden quality, most character- 
istic of fluid. Over the compressed and vicariously distended lung 
above the effusion Skodaic resonance is obtained. 

A small effusion usually affords no physical signs anteriorly, being 
recognized by the appearance of a narrow zone of basal flatness 
posteriorly, which extends from the spine outward toward the axilla, 
and shows, with the patient in an upright position, an upper limit 
following a line of upward convexity. When an effusion attains 



2 8o PHYSICAL DIAGNOSIS 

sufficient volume to produce signs anteriorly, its earliest effects are the 
substitution of flatness for normal hepatic dulness on the right side, and 
for normal tympany in the upper part of Traube's semilunar space, 
according to the side affected. Over a moderate effusion, reaching as 
high, say, as the fourth rib anteriorly, the upper level of the flatness 
follows an undulating line curving from behind forward, somewhat 
in the outline of the letter S — Ellis's "S-shaped line of flatness" 
(Fig. 115). Ellis's line, which corresponds to the line of contact 
between the exudate and the overlying lung, is lowest at the 
spine, whence it runs obliquely upward and forward in an S-shaped 
course toward its summit in the axilla, thence dropping abruptly 
downward and forward to the sternum, where it terminates at a 
slightly higher level than that of its spinal extremity. An effusion 
large enough to cause the foregoing sign usually produces either 
decided vertical extension of the area of hepatic flatness, or very 
definite obliteration of Traube's space, and more or less lateral and 
upward dislocation of the cardiac area. Persistence of tympany in 
Traube's area, despite signs of a left-sided effusion, suggests the 
formation of adhesions whereb}' the fluid is prevented from gravi- 
tating to the bottom of the pleural sinus. 

Except at the base, where defective resonance is not unlikely to 
persist indefinitely, the transition from flatness to impaired reso- 
nance to the normal pulmonary percussion sound rapidly progresses 
over the site of the effusion as it subsides. Persistent areas of flat- 
ness, with absence of tactile vibrations, point to circumscribed per- 
manent thickening of the pleura. Coincidentally with the above 
changes, it is found that the organs displaced by the effusion recede 
to their physiologic percussion limits. 

Movable flatness, due to change in the posture of the patient, is 
rarely demonstrable in simple pleural effusion, and in those excep- 
tional instances in which the change does occur the differences 
in the height of the flatness are very slight and of slow appearance. 
On the contrary, when the pleura contains both fluid and air, as in 
hydropneumothorax, shifting flatness is readily determined. In 
attempting to gage differences in the upper level of flatness by com- 
parison of the surface markings of this limit in the erect and the 
recumbent positions, it is well to remember that the normal stretching 
of the skin when the subject's posture is altered shifts marks made 
thereon, and that apparent postural differences in levels of flatness 
are often referable merely to this resiliency of the integument. 

Grocco's sign, or the presence of a triangular area of shifting dulness 
at the posterior thoracic base opposite the effusion, is a practically 
constant indication of free fluid within the pleural sac (Fig. 115). 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 28 1 

This paravertebral dulness attends both small and large free effusions, 
and can also be detected in encapsulated pockets of fluid lying close 
to the spine; it cannot be demonstrated in interlobar pleurisy. 
Grocco's sign has been attributed partly to mutation of the vertebral 
vibrations by the pressure of the fluid against the spine, and partly 
to dislocation of the mediastinum toward the unaffected side. As 
a rule, the dull area is larger in effusions of the right than in those 
of the left pleural cavity. 

In order to outline Grocco's triangle, the upper limit of the 
effusion and the lower limit of normal pulmonary resonance on 
the opposite side are first ascertained, with the patient in the 



Dulness 
(Grocco's triangle)! 




Upper level of effusion 
(Ellis's line) 



Flatness 



Fig. 115. — Grocco's paravertebral dulness in pleural effusion. Arrows indicate per- 
cussion lines to be followed in mapping out the dull area. 



erect posture. The triangle itself is mapped out by percussing 
downward over the spine, horizontally inward along lines paral- 
lel to the spine, and obliquely inward toward the spine, sur- 
face markings, to be subsequently connected by a line, being made 
at the several points at which resonance is replaced by dulness (Fig. 
115). The vertical side of the right-angle triangle thus erected 
corresponds to the line of the vertebral spines, extending from a 



282 PHYSICAL DIAGNOSIS 

point somewhat higher than the upper level of effusion flatness to 
the lower limit of normal pulmonary resonance ; the base coincides 
with the line of the latter on the unaffected side: the hypotenuse 
is formed by a line (sometimes showing a moderate outward con- 
vexity) joining the extremities of the vertical and base lines. The 
paravertebral triangle disappears or greatly contracts when the 
patient lies upon the affected side, and reappears when the erect 
position is resumed; it is not demonstrable after the removal of 
the effusion. 

Subphrenic abscess may account for a paravertebral triangle of 
dulness on the opposite side, but here the dull area is low and broad, 
and not so prone to be influenced by posture. In lumbar abscess 
Ewart has detected a similar percussion finding that gave way to 
normal pulmonary resonance as soon as the pus was evacuated. 
Ascites sometimes produces a bilateral triangle of paravertebral 
dulness, differing from that due to a bilateral pleural effusion in 
being perfectly symmetric, of greater width, and of lesser height. In 
abdominal cyst paravertebral dulness has been found by Smithies, 
who also noted in pregnancy a roughly triangular dull patch, with 
a flat summit and convex hypotenuse, to the left of the spine. 

Auscultation. — Partial or complete suppression of the respiratory 
murmur is the rule below the upper limit of the effusion, above which 
loud bronchovesicular or bronchial breathing is produced by the com- 
pressed lung. On the unaffected side there is a compensatory exag- 
geration in the intensity of the breath-sounds. Exceptionally, in 
the case of extreme pulmonary compression and bronchial occlusion 
by a massive effusion, practically no respiratory sounds are audible 
over the affected half of the thorax. In contrast to this, there are 
certain effusions, occurring especially in children, over which distant, 
though distinct, tubular or even amphoric respiration is heard, and 
in the face of such findings one must carefully exclude the possibility 
of a coexisting pulmonary consolidation or cavity. 

In general, the voice-sounds are weakened or quite obliterated by an 
effusion, save in those cases which afford bronchial breathing and, in 
consequence, a corresponding degree of bronchophony. The nasal 
bleating of egophony is frequently recognized near the upper level of 
percussion flatness. BaccelWs sign (the transmission of whispering 
pectoriloquy through a serous but not through a purulent exudate) is 
by no means distinctive; the whispered voice is inaudible in many 
serofibrinous as well as purulent effusions. As the volume of the 
fluid diminishes and the natural resiliency of the lung is restored, the 
normal respiratory and voice-sounds gradually reappear from above 
downward, both at the site of the effusion and in the lung above it. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 283 

During the first stage of the process auscultation over the dry, 
inflamed pleura reveals numerous friction-sounds {jrictio indux), 
like those of acute fibrinous pleurisy, though generally of greater 
intensity and wider distribution. When the exudate is poured out 
these sounds, of course, disappear below the upper level of the fluid, 
above which, however, friction may continue to be heard, owing to 
patches of dry pleurisy here coexisting. As the effusion diminishes, 
allowing the roughened pleural surfaces again to rub together with 
respiration, the primary friction-sounds reappear, as the frictio redux, 
and this sign may stubbornly persist for a long period after complete 
resorption has taken place, the sounds possibly acquiring a coarse 
grating or creaking quality suggestive of extensive pleural roughening. 

Diagnosis. — There is no difficulty in recognizing a large effusion 
by this distinctive group of physical signs: unilateral immobility 
and overfulness of the chest, with absence of the diaphragm shadow; 
a zone of basal flatness over which tactile fremitus, vocal resonance, 
and respiratory sounds are abolished, and above which they are 
exaggerated and attended by Skodaic resonance; flatness in Traube's 
space and at one base a paravertebral triangle of shifting dulness; 
and various visceral displacements. 

But the diagnosis is not always so clear as the above paragraph 
implies, for a moderate pleural effusion, particularly in a child, may 
afford two most significant indications of croupous pneumonia — 
bronchophony and bronchial breathing of the most exquisitely tubular 
type; while, on the other hand, there are certain cases of massive 
pneumonia which, by fault of bronchial occlusion, closely ape the 
auscultatory findings of a copious effusion. Though in the doubtful 
case the aspirating needle is usually the court of final appeal, it 
should be recalled that a severe initial chill, high fever, urgent dyspnea, 
herpes, rusty sputum, abnormal pulse-respiration ratio, and absence 
of visceral displacement are in favor of pneumonia. Another most 
important differential point is afforded by percussion, which in 
pneumonia shows that the resiliency appreciated by the pleximeter 
finger is of a much greater degree than that felt in pleural effusion, 
the percussion sound at the same time being of fuller volume and of 
lower pitch over a consolidation. 

Should the diagnosis lie between inflammatory effusion and 
hydrothorax, it is to be recalled that the latter is not attended by 
fever, pain, or friction; that it is more commonly bilateral than 
unilateral; that it is usually associated with dropsy of other parts, 
of which sign some chronic lesion (especially of the heart or the 
kidneys) is the obvious factor. Paracentesis yields in hydrothorax a 



284 PHYSICAL DIAGNOSIS 

fluid of lower specific gravity, smaller albumin content, and less 
coagulability than that due to an inflammatory exudate. (See 
p. 53.) Absence of voice and respiratory sounds and visceral dis- 
placements cannot be taken as criteria of differentiation, being 
common to both conditions; but, as a rule, the basal flatness of 
hydrothorax is capped by a horizontal, not an S-shaped, line. A 
point of some moment is the comparative ease with which movable 
flatness is demonstrable in hydrothorax, as contrasted with the great 
difficulty, usually the impossibility, of distinguishing such a sign in 
an inflammatory effusion. 

In chronic pleural thickening the association of a restricted respira- 
tory excursion, enfeebled breathing, deficient fremitus, and flatness 
at one base gives a close imitation of the physical signs of an effusion. 
But in thickened pleura the chest-wall is likely to be retracted and 
the heart drawn toward the affected side, while the opposite lung may 
be in a state of permanent overinflation; the flatness often acquires a 
peculiarly wooden quality and lacks a clean-cut marginal definition 
and S-curved summit; and no movable dulness alongside the spine 
can be mapped out. In pleural thickening, moreover, there are 
generally evidences of pulmonary fibrosis and a history of some 
primary disease to account for the pleural changes. 

A large pericardial effusion may be distinguished from fluid within 
the left pleural sac by the following differences: in pericardial effu- 
sion the displacement of the heart is upward rather than to the 
right of the sternum; the flatness is roughly pyramidal in shape 
and corresponds to the outline of the distended pericardium, while 
immediately to the left, and perhaps also in the axilla, the percus- 
sion sound is Skodaic. Pulmonary resonance, rather than movable 
dulness, is found at the base posteriorly. Other signs pointing to 
pericardial effusion include apical weakness and basal intensity of 
the cardiac sounds, a feeble and sometimes paradoxic pulse, and 
the existence of dyspnea of a most extreme grade. 

Enlargement of the hepatic area, as from abscess, cancer, or echino- 
coccus of the right lobe, may account for a basal zone of flatness, with 
abolished fremitus and respiratory sounds, thereby suggesting a 
right-sided pleural effusion. But in these conditions the upper 
limit of flatness is likely to be horizontal, convex, or irregular (not 
S-shaped), the overlying lung does not emit Skodaic resonance, and 
the opposite posterior base fails to show a typical Grocco's triangle. 
If perihepatitis exists, it is not unusual also to hear a basal friction- 
sound below the upper boundary of the flatness, while in echinococcus 
disease it may be possible to elicit a distinctive hydatid fremitus. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 285 

Intrathoracic tumors may enfeeble fremitus and respiratory sounds, 
displace the heart, and dull pulmonary resonance so as to counterfeit 
a pleural effusion, except that their physical signs are not affected 
by postural changes, are not uncommonly bilateral, and are generally 
limited to the upper or middle thorax, being, therefore, underlaid 
by a strip of pulmonary resonance at the base. If the neoplasm be 
mediastinal, the signs are usually parasternal and attended by 
characteristic evidences of intrathoracic compression affecting the 
bronchi, esophagus, and great vessels and nerves of the mediastinum. 
The fact that tumors of the lungs and pleura are prone to excite a 
pleural effusion makes their recognition possible, in such instances, 
only after a careful analysis of the case-history and the diagnostic 
use of the aspirator. 

PURULENT PLEURISY (Empyema; Pyothorax) 

Clinical Pathology. — Empyema, or purulent pleurisy, is generally 
secondary to some preexisting focus of infection, but exceptionally it 
is of primary origin, especially in children. The effusion may be puru- 
lent from the beginning, or the suppuration may be due to the contam- 
ination of a serofibrinous effusion (rarely, a dry, fibrinous pleurisy) 
by the bacteria of suppuration. In children pneumococcus infec- 
tion, primary or metapneumonic, is the most active factor of puru- 
lent effusions, while in adults the streptococcus, pneumococcus, 
and tubercle bacillus, in this order of frequency, are the most 
common exciting causes (W. Watson Cheyne). Pneumococcus 
empyemas are more prone to spontaneous absorption than those 
due to other bacteria, with the possible exception of the bacillus of 
Eberth, as noted by Gerhardt, while purulent effusions referable 
to mixed infections are usually of graver character than those pro- 
voked by a single variety of microorganism. In establishing the 
origin of an empyema these factors should be rehearsed: pneumonia, 
tuberculosis, and other infectious processes of the lungs; infection by 
way of the blood- and lymph-vessels, as in the specific infections and 
in local lesions not directly contiguous to the pleurae; and infection 
by erosive and gangrenous processes of the esophagus, stomach, liver, 
ribs, and vertebrae. Septic wounds of the chest account for some 
cases of empyema, which also can arise as a consequence of faulty 
asepsis during paracentesis. 

The pathologic changes of empyema differ chiefly in degree from 
those of non-suppurative pleurisy, than which the former works the 
more serious damage. The character of the effusion is exceedingly 
variable, ranging from a thin, moderately opaque seropurulent liquid 



286 PHYSICAL DIAGNOSIS 

of yellowish-green hue to a thick, creamy, yellow pus, the former 
separating on standing into a thin zone of leukocytes overlaid by a 
considerable quantity of clear serum, and the latter being of homo- 
geneous consistence. In fetid cases the exudate emits a most offensive 
stench, and may have a brownish color. Fibrin, in the form of flakes 
or larger masses, is distributed through an empyematous effusion 
in variable amounts, the exudate in some cases being of a most decided 
fibrinopurulent nature. Microscopically, leukocytes are the most 
important constituent of the exudate, whose degree of purulence is 
proportionate to its richness in these cells; a variable number of 
erythrocytes, degenerate endothelium, fat-globules, and cholestenn 
crystals are also found, together with one or more of the varieties 
of bacteria mentioned above. 

The pleural surfaces are actively inflamed and thickened by newly 
proliferated vascular connective tissue and by extensive leukocytic 
infiltration; they are covered with a dense, friable, grayish-yellow 
pseudomembrane or with a granulating pyogenic membrane; and 
sometimes show circumscribed areas, single or multiple, of necrosis. 
Through such breaches in the integrity of the pleura the pus 
spreads to other parts, whence it may, by the erosion of fistulous 
channels, find spontaneous evacuation — empyema necessitatis. The 
formation of a fistula between the pleura and a bronchus means 
the establishment of a pyopneumothorax; in other instances the pul- 
monary parenchyma becomes the seat of abscess or of extensive 
gangrenous destruction, these changes being especially prone to 
supervene in virulent putrid empyemas. Fistulation through an 
intercostal space, with discharge of the pus through the chest-wall, 
is also a common method of spontaneous evacuation. Less fre- 
quently the pus burrows into the esophagus, the stomach, the peri- 
cardium, the opposite pleura, the peritoneum, or even into such remote 
parts as the kidney, the lumbar region, and the groin, but only in 
most exceptional cases has this been observed. 

Pulsating pleurisy, in which pulsations synchronous with the sys- 
tolic impulse of the heart are palpable and generally visible in the 
intercostal spaces, particularly of the upper left chest, is a rare physical 
sign in pleural effusion. (See Fig. 125, p. 329.) It is met with 
especially in empyema (pulsating empyema), both as a true intra- 
pleural pulsation and as a throbbing tumor in empyema necessitatis; 
it is seen exceptionally in non-purulent effusions, and occasionally it 
is found in connection with a coexisting pneumothorax. 

The mechanism of pulsating pleurisy has long been a moot point. 
Calvert logically explains the phenomenon by showing that the pleural 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 287 

wall, distended by fluid and bordering upon a collapsed lung, lies 
in close contact with the thoracic aorta whose systolic expansions 
are taken up by the pleural wall and thereby transmitted to its weak- 
est portion. If this happens to be external, its rhythmic stretching 
with each increment of pressure produces visible pulsations, syn- 
chronous with cardiac systole, upon the overlying surface of the chest. 

The visceral displacements occurring in empyema are similar to 
those of a serofibrinous effusion, but they are usually more striking, 
owing to the greater weight of the purulent liquid; this factor plus 
the soft, relaxed state of the parietal structures around an empyema 
accounts for a relatively greater depression of the diaphragm and 
a more decided distention of the thoracic wall in this form of pleural 
effusion. 

After the removal of the exudate, either instrumentally or spon- 
taneously by absorption or by evacuation, the pleural surfaces con- 
tinue to produce pus for a protracted period, and when this finally 
ceases, they are left irreparably injured. The damage is moderate 
in some cases, but in others there is inordinate pleural thickening 
with extensive pulmonary fibrosis, ultimately leading to contraction 
of the lung and to deformity of the affected side. (See Fig. 38.) 

Physical Signs. — The physical signs of empyema do not differ 
materially from those of serofibrinous pleurisy, in so far as palpation, 
percussion, and auscultation are concerned, the findings afforded 
by these methods of research being identical, whether the effusion 
consists of serum or of pus. But inspection, at least in certain 
instances, furnishes signs of sufficient distinction to warrant separate 
mention, in view of the difficulty in discriminating between these 
two types of effusion, without resort to the aspirating needle. 

In a severe case the dyspnea is most striking, and the patient's 
appearance betokens grave sepsis — anemic pallor, a hectic flush, 
sordes, mental apathy, low delirium, great prostration and emacia- 
tion, remittent fever, and recurrent drenching sweats. The enlarge- 
ment of the affected side of the thorax is generally more noticeable 
than in an ordinary serofibrinous effusion, and the interspaces, 
instead of being merely obliterated, may even bulge outward between 
the ribs. Unilateral enlargement of the chest is common in 
children, owing to resiliency of the thorax, but this is not 
perceptible in adults, because of the rigidity of the mature thorax. 
The tissues of the chest-wall are sometimes boggy and edematous, 
and there may be either a discolored local area of distinct fluctuation 
that betrays the prefistulous stage of an empyema necessitatis, or, 
indeed, the fistula itself. The cardiac and the hepatic displacements 



2 88 PHYSICAL DIAGNOSIS 

are likely to be more conspicuous than in serofibrinous cases, and 
the excessive weight of a copious empyema is capable of depressing 
and pushing forward the diaphragm to such an extent as to produce 
a well-marked tumor in the hypochondrium of the affected side. 
As a rule, Grocco's sign is strikingly shown in purulent effusions, 
and tubular breathing, rather than respiratory silence, is more com- 
mon than in serofibrinous pleurisy. 

In the vast majority of instances the differentiation of empyema 
and the other forms of pleural effusion can be made only by explora- 
tory puncture, for which no other method of physical diagnosis is 
a satisfactory substitute. 

Pulsating pleurisy may, at first glance, suggest aneurism of 
the aortic arch, but in the former the pulsations lie far outside the 
course of the aorta — between the third and fifth interspaces on the 
anterior or lateral surface of the thorax, almost invariably on the left 
side, and exceptionally behind; moreover, the thrill, bruit, cardio- 
vascular changes, and pressure symptoms of aneurism are wanting. 

CIRCUMSCRIBED PLEURISY 

Aside from the local dry pleurisies and the free effusions just 
discussed, there are other pleuritides restricted to certain local areas 
of the pleural sac and which, because of this peculiarity, present 
physical signs difficult to appreciate and to interpret. Of these 
circumscribed types of pleuritis, the diaphragmatic, the encapsulated, 
and the interlobar deserve special consideration. 

Diaphragmatic Pleurisy. — This type of pleural inflammation, 
implicating the pleural investments of the diaphragm and the lower 
pulmonary surface, is commonly attended by a serofibrinous effusion, 
though rarely the exudate is purulent, and exceptionally the process 
consists of a- fibrinous or plastic inflammation. The condition is 
by no means of frequent incidence, in comparison with the ordinary 
forms of pleural effusion. 

The physical signs of diaphragmatic pleurisy are usually over- 
shadowed by the subjective symptoms, in view of which the diagnosis 
must rest chiefly upon the symptomatology of the onset and upon 
the character of the intense pain that monopolizes the clinical picture. 
The onset, which is most likely to be sudden, may begin with a chill, 
considerable fever, dyspnea, and perhaps vomiting. The pain, 
largely due to phrenic irritation or neuritis, is referred to the lower 
thoracic and the upper abdominal regions, particularly to the hypo- 
chondrium and epigastrium. Exquisite tenderness is elicited by 
pressure over the line of the diaphragm between the end of the tenth 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 289 

rib and the ensiform cartilage, and also along the course of the 
phrenic nerve in the supraclavicular space at the outer border of the 
sternocleidomastoid muscle and often in the intercostal spaces at 
the sternal border. The pain is naturally much aggravated by the 
movements of respiration, and by the hiccough and vomiting that 
prove such distressing symptoms in many cases. The abdomen, 
though not distended, is acutely sensitive and resistant, especially 
on the side of the pleurisy. 

Owing to the great pain the respiratory excursion is restricted and 
the breath-sounds are suppressed on the affected side, upper thoracic 
respiration being a conspicuous sign on inspection. Exceptionally, 
dry friction-rubs are audible in the region of the diaphragm, and if 
there be a fairly large effusion, a basal zone of flatness, with more or 
less depression of the liver or the spleen, may also be made out. Such 
visceral displacements are particularly prone to occur if the effusion 
be purulent, and in such an event one should look for edema of the 
chest-wall and for bulging of the lower interspaces. 

Because of its violent onset, decided constitutional disturbances, 
and active abdominal symptoms, diaphragmatic pleurisy must be 
carefully distinguished from certain forms of the "acute abdomen," 
notably those due to gall-stone colic, to appendicitis, and to acute 
peritonitis, and in making this discrimination due weight must be 
given to the clinical history of the case in question. This having 
been analyzed, one may also succeed in detecting the basal friction, 
the typical areas of tenderness, and the unduly striking dyspnea, 
which together point surely to diaphragmatic pleural inflammation. 

Encapsulated or Encysted Pleurisy. — In this variety of effusion, 
which is more commonly purulent than serofibrinous, the exudate, 
instead of being free in the pleural cavity, is limited by inflammatory 
adhesions to circumscribed areas, the fluid being thus walled off into 
a single encapsulated collection or into several pockets, either dis- 
tinct and separate or communicating. The aspirating needle is the 
only certain means of detecting effusions of this sort, though their 
existence is suggested by the discovery of circumscribed physical 
signs of fluid. 

Interlobar Pleurisy. — This term is applied to a type of local pleurisy 
in which the exudate, poured out by the inflamed pleural reflections 
between the lobes of the lungs, is confined by adhesions to the inter- 
lobar surfaces. A circumscribed exudate of this sort, which may be 
either purulent or serofibrinous, is commonly limited to the septum 
between the right upper and middle lobes, and, like other forms of 
walled-off effusion, usually cannot be diagnosed without resort to 



290 PHYSICAL DIAGNOSIS 

aspiration. In interlobar empyema the pus sometimes fistulates 
into a neighboring bronchial tube, such an accident being betrayed 
by paroxysmal cough productive of a variable quantity of purulent 
sputum. 

The physical signs of an interlobar effusion should be sought for 
along the course of the interlobar septa, the findings being sharply 
restricted to these lines if the fluid be near the surface, but being 
well below them if the process be deep. Circumscribed tender- 
ness, absence of tactile fremitus and voice-sounds, pleural friction, 
feeble respiration, and dulness bordered by Skodaic hyperreso- 
nance, when localized near the levels of the fourth and fifth ribs^ 
either anterolateral^ or posteriorly, are suggestive findings that 
the Rontgen-ray and the exploring needle may clothe with cer- 
tainty. 

Mediastinal Pleurisy. — Effusions into the mediastinal space are 
of rare occurrence and ordinarily represent a postpneumonic com- 
plication, or they may be secondary to tuberculosis, to pulmonary 
abscess, or to an encysted diaphragmatic pleurisy. As a rule, such 
effusions are purulent rather than serofibrinous. The physical 
signs relate conspicuously to mediastinal pressure, consisting of the 
sudden onset of fever, substernal pain, dyspnea, and cough, and 
later, as the oppression becomes aggravated, orthopnea, rapid 
respiration, suffocative cough, dysphagia, laryngeal spasm, hoarse- 
ness, aphonia, and extensive congestion of the surface veins de- 
velop. Apart from this "mediastinal syndrome," the objective 
findings are in no wise distinctive: they consist of an abolition of 
vocal fremitus, impaired resonance, and absent respiratory sounds 
in one infrascapular region, contrasted with intense percussion 
resonance, and perhaps bronchial respiration at the apex on the 
same side, with compensatory hyperresonance over the opposite 
lung. Aspiration is likely to fail as a diagnostic aid, because of the 
depth of the lesion and the density of the overlying lung. 

CHRONIC ADHESIVE PLEURISY (Chronic Plastic or Fibrinous Pleurisy; 
Symphysis Pleurae) 

Clinical Pathology. — As a rule, this variety of pleurisy is a sequel 
of pleural effusion, beginning as an organization of the fibrous deposit 
left upon the pleural surfaces after the removal of the fluid exudate; 
less commonly it represents an agglutination and fibrosis of the 
pleurae, secondary to an acute plastic pleurisy or developing as a slow,, 
insidious, progressive lesion at no time betrayed by active symptoms. 
The visceral and parietal pleurae are unduly thickened and inti- 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 29 1 

mately united by dense fibrous masses, which, if there be sufficient 
respiratory movement, tend finally to yield to the incessant traction, 
whereby they are converted into tough interpleural cords; or the 
cicatricial overgrowth may weld the two pleural membranes into a 
single fibrocalcareous layer, sometimes so extensive as practically to 
obliterate the pleural cavity, especially if the corresponding lung be 
also diseased. In some instances there are small intrapleural loculi 
of fluid, in others traction bronchiectases develop, and in still others 
the lung becomes encapsulated by a rigid, contracting pleural invest- 
ment. In consequence of the pleural lesions the excursion of the 
lung is limited and its function hampered; the pulmonary tissue 
undergoes extensive compression and fibrosis, the septa are pene- 
trated by fibrous bands, interlobar agglutination may unite two or 
more lobes, and firm adhesions commonly develop, particularly 
at the bases and at the apices posteriorly. Exceptionally, chronic 
adhesive pericarditis and proliferative peritonitis coexist. 

Physical Signs. — Inspection. — In the average case one finds 
little else than a moderate degree of dyspnea, with slightly impaired 
mobility of the chest on the affected side, and not infrequently even 
such clues are wanting. But when the pleurae are extensively impli- 
cated, the dyspnea becomes most striking, the respiratory movements 
are greatly hampered, the affected side expands but little, if at all, and 
may show a circumscribed area of flattening or retraction. (See Fig. 
45, p. 93.) In cases following empyema the scar of the fistulous drain 
at once arrests the examiner's attention, and it is in examples of 
this kind that local deformities of the thorax, with drooping of the 
shoulder, overlapping of the ribs, and spinal deflection, become most 
conspicuous. (See Fig. 38, p. 90.) The heart may be drawn to the 
right or to the left, according to whether the traction is exerted by 
right- or by left-sided adhesions, and in old unilateral lesions com- 
pensatory enlargement of the opposite half of the chest tends to 
supervene. Apical adhesions that irritate the first thoracic sympa- 
thetic ganglion are betrayed by unilateral sweating or flushing of the 
face and by dilatation of the pupil. Evidences of venous stasis, 
from dilatation of the right heart, may appear late, in cases of great 
chronicity, and in such instances one commonly observes a network 
of delicate venous radicles curving across the lower anterior thorax. 

Palpation. — The intensity of tactile fremitus varies with the 
peculiarities of the lesion in the individual case: it is ordinarily 
enfeebled or abolished over areas of simple pleural thickening, but 
despite this barrier to voice vibrations, the fremitus may be clearly 
conducted to the surface by bands of compact pleuropulmonary 
adhesions. Friction fremitus, of a coarse, grating quality, is appre- 



292 PHYSICAL DIAGNOSIS 

ciable over patches of mobile pleural roughening. In moderately 
advanced cases the hand is more useful than the eye in detecting 
respiratory immobility, particularly circumscribed, of the chest-wall. 

Percussion. — The thicker the pleurae and the greater the pulmonary 
fibrosis, the less resonant the percussion sound over the parts affected. 
Resonance may be simply impaired, as shown by a slightly elevated 
pitch, shortened duration, and increased resistance; or there may 
be dulness of a peculiar wooden character, with most striking resist- 
ance to the pleximeter finger. Emphysematous percussion sounds 
over the opposite lung are familiar findings in advanced cases. 

Auscultation. — The respiratory murmur and vocal resonance are 
enfeebled, especially at the base, in proportion to the degree of pleural 
thickening, of respiratory restriction, and of vesicular obliteration. 
Aside from these findings, many cases show the auscultatory changes 
of such coexisting processes as pulmonary fibrosis and emphysema, 
bronchitis, and bronchiectasis (q. v.). Friction, if audible, is gen- 
erally loud, leathery, and creaking. 

Diagnosis. — The association of thoracic deformity and immo- 
bility with such signs as enfeebled breathing, diminished tactile 
fremitus, wooden dulness, and coarse friction makes a well-developed 
adhesive pleurisy an easily recognized condition. In doubtful cases, 
presenting a less clear-cut symptomatology, the patient's history and 
the careful study of the respiratory murmur and the percussion find- 
ings are to be relied upon as the chief diagnostic clues. 

HYDROTHORAX (Pleural Dropsy) 

Hydrothorax, or dropsy of the pleural cavity, is usually part and 
parcel of an anasarca due to chronic cardiac, renal, or hepatic dis- 
ease or to high-grade anemia. The effused fluid is a simple clear 
transudate, of lemon-yellow color, poor in cellular elements, and con- 
taining little or no fibrin; the specific gravity rarely exceeds 1015, the al- 
bumin content is not more than 20 or 30 grams, and the formed elements 
are chiefly endothelial cells shed by the pleural surfaces. (See p. 53.) 
Here may be noted Peju's observation, that pleural dropsies occurring 
in subjects of anthracosis may consist of thin black fluid charged 
with carbon particles. Hydrothorax is generally bilateral, though 
unilateral effusions are also met with, chiefly in connection with 
chronic cardiac disease, in which right-sided hydrothorax, frequently 
preceding a general edema, is the rule, probably because of pressure 
on the vena azygos major by an enlarged right auricle (Baccelli). 
When stasis thus provoked extends to the vena azygos minor, effusion 
into the left pleural sac occurs, and in this manner a bilateral hydro- 
thorax is established, the volume of which is usually greater on the right 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 293 

side. Pressure by the dilated heart upon the pulmonary veins is the 
explanation of cardiac hydrothorax given by Fetterolf and Landis. 
In certain cases of Laennec's cirrhosis there is also a tendency toward 
right-sided hydrothorax, attributable, at least in part, to azygos 
compression by the enlarged veins of the esophageal plexus (Martini) . 
Unilateral hydrothorax may be associated with local lesions of the 
same side (neoplasm, fibrosis, aneurism) that compress the great 
vessels at the pulmonary radix; it sometimes affects the free pleural 
sac opposite the one obliterated by universal adhesions; it occurs 
rarely (as " hydrops ex vacuo") in the pleuropulmonary space created 
by the recession of a tightly contracted lung; and it may exist as a 
loculated collection of fluid walled off by impermeable adhesions. 
In pure hydrothorax the pleural surfaces are not inflamed, though 
this change tends to supervene as the result of the chronic conges- 
tion, and the primary transudate, in such an event, acquires many 
of the characteristics of an inflammatory exudate. 

The physical signs are those of intrapleural fluid, generally bilateral, 
unattended by pain and friction, and associated with clear evi- 
dences of the underlying disease. Dyspnea and cough in a dropsical 
subject should always prompt a search for fluid within the pleural 
sacs. The differences between the physical signs of hydrothorax 
and an inflammatory pleural effusion have been described under 
the latter. (See p. 283.) 

HEMOTHORAX (Pleural Hemorrhage) 

Hemothorax, or hemorrhage into the pleural cavity, results from 
accidents such as traumatism of the chest, rupture of an aneurism, 
erosion of a blood-vessel, and free vascular oozing incident to the 
hemorrhagic diathesis. The extravasated blood coagulates, the 
serum is rapidly absorbed, and the clot is deposited upon the most 
dependent surface of the pleura, whence, if uninfected, it is even- 
tually removed by absorption, without giving rise to pleural inflam- 
mation. Infection, however, is not unlikely to take place, partic- 
ularly in hemothorax due to wounds of the chest-wall or secondary 
to some erosive lesion that establishes a fistulous communication 
with the gullet or the larger air-passages, and in such cases the prompt 
onset of a purulent pleurisy is to be expected. 

The physical signs relate to a rapidly accumulating pleural effusion, 
with or without evidences of actual pleuritis. These findings, cor- 
related with the patient's clinical history and with the objective 
symptoms of acute hemorrhage and shock, are generally sufficient 
to warrant the diagnosis of hemorrhage into the pleural cavity. 



2 o4 PHYSICAL DIAGNOSIS 

CHYLOTHORAX (Hydrops Chylosus) 

Chylothorax, or the presence of an effusion of chyle in the pleural 
sac, is a very rare affection, arising in consequence of a leakage of 
chyle from the thoracic duct or from a large intrathoracic lymphatic 
trunk. This accident may be of traumatic origin, or may be due 
to cancerous erosion, to lesions of the lymph-vessels, or to left sub- 
clavian venous thrombosis; rarely, it has been ascribed to filariasis. 
The effused fluid consists of a turbid, creamy emulsion of fat, 
having either a faintly sweetish odor or none at all, being peculiarly 
resistant to decomposition, and clearing on shaking with ether, but 
not doing so on centrifugalization. The specific gravity of the 
transudate ordinarily ranges between 1015 and 1020, and it contains 
approximately from 3 per cent, of albumin to twice this amount 
or more, together with a variable sugar content, and, inconstantly, 
fibrin and casein. 

The physical signs of chylothorax are those of a pleural effu- 
sion, either unilateral or bilateral, and the diagnosis must be 
made by thoracentesis. True chylous hydrops, rather than a chyli- 
form effusion, is indicated by aspirating a creamy fluid yielding at 
least 0.2 per cent, of sugar, abundantly charged with very minute 
fat-droplets, and containing relatively few cellular elements. In 
contrast, a chyliform effusion shows a lower sugar content, fewer 
and larger fat-particles, and a greater number of degenerate cells. 
When both types of effusion coexist, as is sometimes the case, 
examination of the fluid is obviously of no avail, and in this con- 
tingency the differentiation, if one can be made, must needs rest 
largely upon the case history. Chylothorax is suggested when it is 
possible to identify some factor of chyle leakage: trauma, cancer 
of the pleura, thrombosis of, the left subclavian vein, or, possibly, 
filarial infection; while chyliform effusions, though also met with 
in pleural cancer, are likely to be associated with severe anemias, 
tuberculosis, chronic cardiac disease, and grave cachectic states. 
(C/. Chyliform Pleurisy, p. 276.) 

PNEUMOTHORAX (Hydropneumo thorax? Pyopneumo thorax; Hemo- 

pneomothorax) 

Clinical Pathology. — Pneumothorax, or the accumulation of air 
within the pleural cavity, is generally attended by an effusion of 
serum, pus, or, rarely, blood, and hence the more specific terms, 
hydropneumothorax, pyopneumothorax, and hemopneumothorax are 
appropriate, according to the character of the fluid. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 295 

Owing to the elastic tension of the lungs, the normal pressure 
within the pleural cavity (754 mm. of Hg) is about 6 mm. lower 
than that of the pulmonary vesicles and air-passages (760 mm. of 
Hg.), and in consequence of this difference, designated as "negative 
intrapleural pressure," the lungs are kept in close contact with the 
inner thoracic wall and the two pleural surfaces are intimately approxi- 
mated. So soon, however, as a communication is established 
between the atmospheric air and the pleural sac, the latter sucks 
in sufficient air to satisfy its negative pressure, or, in other words, to 
equalize the intrapleural and the intrapulmonary pressures. In 
consequence, the lung, by virtue of its inherent elasticity, immediately 
recoils from the chest-wall and contracts, for its so doing is not now 
prevented by a high intrapulmonary tension, and the pleural cavity, 
whose membranes are no longer opposed, is widely distended by 
the aspirated atmospheric air. This constitutes pneumothorax. 
That pneumothorax does not invariably follow pleurotomy is due to 
increased pressure, referable to strong respiratory efforts, within the 
corresponding lung, whereby its contractility is overcome and the 
organ becomes overdistended. This not only insures adequate 
approximation of the two pleural surfaces, but may even cause pro- 
trusion of the lung through the breach in the chest-wall, and thus 
produce a pulmonary hernia. 

Air enters and accumulates within the pleural cavity in conse- 
quence of numerous different factors, of which pulmonary tuberculosis 
is by all odds the most common. Fully 90 per cent, of all pneumo- 
thoraces are due to this cause (Weil; West; Walsh), the entrance 
of air usually being through a breach made in the pleura by a small 
interpleural or subpleural tubercle, or, less frequently, through the 
rupture of a pulmonary cavity lying immediately beneath the pleura. 
The favorite site of such perforations is toward the base rather than 
the apex of an upper lobe, especially on the left side. Empyema 
is also an important cause of pneumothorax, and in this disease 
the air commonly gains access through a bronchopleural sinus, 
while only exceptionally does it enter by the fistulous tract in the 
chest-wall created by an empyema necessitatis. Other destructive 
diseases that may produce pneumothorax, by the erosion of a fistula 
into the lung and bronchial tubes, include abscess, gangrene, cancer, 
and hydatid cyst of the lung, suppurative tracheobronchial adenitis, 
and bronchiectasis; while in certain instances the condition is refer- 
able primarily to esophageal erosion, to similar disease of the parietal 
structures, and to ulcerative lesions beginning in a subphrenic 
viscus (stomach, liver, intestine) and ultimately perforating the 



296 PHYSICAL DIAGNOSIS 

pleura, as a rule, after first invading the corresponding lung. Pneu- 
mothorax has been known to follow violent respiratory effort and 
severe muscular strain, the stress of which is sometimes sufficient 
to rupture even a healthy lung, though more often a lung thus torn 
is found to be the seat of latent tuberculosis, emphysematous bullae, 
infarction, or some other lesion that weakens its texture. Violent 
contusions and penetrating wounds of the chest-wall also account 
for the entrance of air into the pleural sac, and to the latter so-called 
traumatic type of pneumothorax the bungling use of the aspirating 
needle occasionally contributes a case. In an exceptional instance 
the pleural cavity fills with gas evolved by the B. aero genes capsulatus 
growing in a pleural exudate. 

Save for rare exceptions, the disease is unilateral; and the collec- 
tion of air fills and thoroughly permeates the free space within one 
pleural sac — general or complete pneumothorax; occasionally, the air 
is circumscribed, by air-tight adhesions, to a part of the pleural cav- 
ity — circumscribed or limited pneumothorax; simultaneous distention 
of both pleural spaces, or bilateral pneumothorax, is a rare clinical 
curiosity in which the subject's life is a matter of hours. If the 
fistulous tract leading to the pleural cavity be patent and permits 
the free passage of air into and out of the pleural chamber, an open 
pneumothorax exists, and in this variety of the disease the intra- 
pleural and atmospheric pressures are equal. Should the orifice 
become sealed, as by adhesions or by a bit of lymph, a closed pneu- 
mothorax is established, in which the intrapleural pressure either 
remains atmospheric or gradually becomes negative, if the excess 
air be finally absorbed. An opening provided with a valvular 
mechanism, which admits air with inspiration, but prevents its 
free escape with expiration, distinguishes a valvular or ventilated 
pneumothorax, a type associated with exceedingly high intrapleural 
tension. Primarily, the great proportion of all pneumothoraces are 
valvular, but the type of the disease is subject to change from time 
to time, because of the readiness with which structural alterations 
in the fistulous opening take place. 

The immediate effect of pneumothorax is a great distention of the 
chest on the affected side, and on puncture of the pleural sac the 
air may escape with considerable force, if positive intrapleural 
pressure exists. If free, the lung on the diseased side is collapsed, 
contracted, and compressed, lying in a small, carnified mass along 
the vertebrae; if the lung be bound down by adhesions, it shrinks 
in a more irregular manner, according to the situation of the bands 
of traction. The mediastinum and its contents, unless firmly 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 297 

anchored by adhesions, are displaced toward the sound side by the 
higher pressure in the pneumothoracic pleura; and by a similar 
mechanism the diaphragm, with the liver and spleen, is unduly 
depressed. Pleural effusion is an almost constant sequel in subjects 
that survive, the exudate being, in order of frequency, serofibrinous, 
purulent, or, exceptionally, hemorrhagic. 

Physical Signs. — Inspection. — The affected side is distended 
and immobile, the intercostal spaces being effaced and the diaphragm 
shadow abolished, while in contrast to this the opposite half of the 
thorax shows exaggerated respiratory movements. The visible 
cardiac impulse is displaced toward the sound pleura, and the liver 
may bulge outward below the right costal margin. Distressful 
dyspnea, paroxysmal cough, cyanosis, rapid feeble pulse, and a 
state of suffocation and collapse are notable objective symptoms of 
acute general pneumothorax, but in cases of long standing the urgency 
of these signs is greatly modified. 

Fluoroscopic examination reveals an abnormally clear and bright 
appearance of the affected side, with contrasting shadows of carnified 
lung above and of fluid below, in case these attendant conditions 
be sufficiently developed to obstruct the passage of the rays (Fig. 
116). The mediastinal shadow lies far from its natural site, and 
the diaphragm is depressed and unnaturally immobile. In some 
cases the phrenic vault shows a downward convexity, and the 
normal inspiratory fall and expiratory rise of the diaphragm are 
reversed. If the displacements be unusually striking, as is the 
tendency in valvular pneumothorax with excessively high tension, 
practically nothing is seen with the fluoroscope save the clean-cut 
shadows of the ribs and clavicle against a bright background corre- 
sponding to the boundaries of the distended pleural sac. 

Palpation. — Vocal fremitus is diminished or entirely lost over the 
air-distended pleura, though toward the apex there may be intense 
voice vibrations referable to pulmonary compression or consolida- 
tion. The liver, in right-sided pneumothorax, is palpable far below 
the costal margin, the displacement of this organ being, as a rule, 
much more conspicuous than in a simple fluid effusion within the 
pleura. Succussion fremitus (v. i.) is occasionally palpable when 
the pleura contains both air and fluid. 

Percussion. — Generally, the percussion sound is unduly loud, sonor- 
ous, and hyperresonant; sometimes it is dull, muffled, and toneless; 
and exceptionally it is tympanitic or even amphoric. Normal pul- 
monary resonance, although rare, is not incompatible with the 
lesion in question. These differences, which relate to the typical 



298 



PHYSICAL DIAGNOSIS 



instance of general pneumothorax, are determined mainly by 
the degree of intrathoracic pressure existing in the individual 
case, and the character of the percussion sound serves to index 
the resiliency of the thoracic wall. Thus, despite the impracti- 
cability of differentiating the three forms of the disease by per- 
cussion alone, it is true that in valvular and in closed pneumo- 
thorax one expects to rind sonorous hyperresonance or muffled 
dulness, according to whether the pressure be moderate or extreme; 




Fig. 1 1 6. — Radiograph of a left pneumothorax. Posterior aspect showing 
shadow of consolidated lung above the air-distended pleura. (Plate by Dr. W. F. 
Manges.) 

while in open pneumothorax, where the intrapleural pressure is 
merely atmospheric, there may be the proper relaxation of the parietes 
to afford tympany. Cracked-pot resonance with Wintrich's sign 
may be elicited over a pneumothorax communicating with a patu- 
lous bronchus. The percussion resistance also varies with the 
elasticity of the chest- wall: commonly, a sort of "air-cushion" sensa- 
tion is felt by the pleximeter finger, but should the tension be exces- 
sive, the resistance is almost board-like. The percussion sounds, 
whatever be their exact quality, are readily distinguishable from 
those found over the opposite — and perhaps vicariously hyper- 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 299 

resonant — lung, and their extension beyond the median and infe- 
rior limits of the normal pleura is readily determined. 

The coexistence of fluid is revealed by a basal zone of flatness 
which readily shifts with changes in the subject's posture, this sign 
of movable flatness being much more evident and easy to detect 
in pneumothorax with fluid than in uncomplicated hydrothorax 
or in inflammatory effusion. 

Auscultation. — Over the distended pleura the respiratory murmur 
is suppressed, often to the point of absolute silence; if at all audible, 
the breathing possesses a far-away amphoric tone or a distant bron- 
chial quality, should the sound transmission travel by way of a 
patch of compressed lung abutting upon an open bronchial tube. 
Vocal resonance is distant and frequently amphoric and echoing. 
Over the unaffected side the respiratory and the voice-sounds are 
puerile and abnormally loud. 

Four noteworthy adventitious sounds should be sought for in 
pneumothorax: the succussion splash (succussio Hippocratis) of 
Hippocrates; the coin sound (bruit oVairain) of Trousseau; the 
metallic tinkle (gutta cadens) of Laennec; and the pulmonary fistula 
sound {water-whistle noise) of Riegel. These important signs, indi- 
cating both air and fluid within the pleural sac, have been described 
in a preceding section, and, therefore, require no further comment 
in this connection. (See p. 169 et seq.) Other abnormal sounds, 
developed by the acts of coughing and deep respiration, consist of 
a medley of bubbling rales of ringing, metallic quality and of 
pleural, pulmonary, and bronchial origin. 

The abnormal situations of the cardiac and hepatic percussion 
areas are generally well defined, especially in cases associated with 
excessively high intrapleural pressure: for example, a valvular pneu- 
mothorax, if left sided, may entirely obliterate cardiac dulness to the 
left of the midsternal line, or, if right sided, may depress the liver 
so that its upper border of dulness is at, if not below, the arch of the 
ribs. To a less striking degree the splenic area is depressed by the 
pressure of air within the left pleural cavity. In left pneumothorax 
Calvert has noted that an apex-beat invisible in recumbency becomes 
apparent when the subject leans forward so as to allow the mobile 
heart (for its pulmonary support is lost) to swing forward against 
the chest- wall. 

Diagnosis. — The sudden onset of urgent dyspnea, cyanosis, and 
collapse is a most significant indication of acute general pneumo- 
thorax, particularly if this syndrome be observed in a phthisical 
subject. The principal confirmatory signs comprise unilateral dis- 



300 PHYSICAL DIAGNOSIS 

tention, immobility, and hyperresonance of the thorax; diminished 
or absent vocal fremitus and resonance; abolished or distantly 
amphoric respiratory sounds; and remarkable displacement of the 
heart, liver, and diaphragm. If an effusion also exists, shifting 
dulness at the base will be found, as well as the peculiar ringing and 
metallic sounds so distinctive of air and fluid within a pleural sac. 
A circumscribed partial pneumothorax may afford no distinctive 
signs whatever — the so-called "mute pneumothorax" of Sabourin. 

Pleural effusion, either exudative or transudative, is sometimes 
suggested by a pneumothorax attended by a collection of intra- 
pleural fluid of sufficient volume to cause an extensive basal area or 
flatness, overlaid by dull hyperresonance and provocative of con- 
siderable visceral displacement; the fact that tubular or amphoric ■ 
breathing above and respiratory silence below may be common to 
both conditions makes their discrimination still more difficult. 
In hydropneumothorax or pyopneumothorax, however, the thoracic 
distention is much more decided and the visceral displacements are 
more conspicuous than in simple effusion; the basal flatness has a 
perfectly horizontal upper level that readily shifts when the patient's 
position is altered; and such important auscultatory findings as 
the succussion sound, metallic tinkling, and the coin sound are 
generally demonstrable. 

Certain cases of unilateral emphysema, secondary to wide-spread 
fibrosis of the opposite lung, in the course of time produce an enlarge- 
ment of one-half of the thorax, which, on percussion, emits a sound 
whose intense hyperresonance is comparable to that found in pneumo- 
thorax, and in the face of such findings the presence of dyspnea, 
cyanosis, and cough makes the resemblance still closer. But despite 
these similarities, the differentiation is not difficult, when one con- 
trasts the vertical excursions of the thorax, the expiratory type of 
dyspnea, and the attenuated (though still vesicular) respiratory 
murmur of emphysema with the thoracic immobility, the desperate 
suffocation, and the respiratory silence of pneumothorax. If these 
fundamental differences prove inadequate, the condition of the 
lung opposite the hyperresonant side and the presence of definite 
pneumothoracic adventitious sounds may furnish conclusive evidence. 

One must occasionally distinguish circumscribed pneumothorax 
from a large superficial pulmonary cavity, owing to the resemblance 
between the percussion tympany and the metallic rales elicited in 
the two affections. A pulmonary excavation, rather than pneumo- 
thorax, is indicated by localization of the physical signs at or near 
the apex of the lung, by the presence of a circumscribed area of 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 301 

intercostal immobility and retraction in this situation, and by finding 
little or no dislocation of the cardiac apex, which, if abnormally placed, 
is drawn toward — not pushed away from — the lesion. Additional 
evidence in favor of a cavity includes intense vocal fremitus, distinct 
pectoriloquy, and loud amphoric or cavernous breath-sounds, in 
contradistinction to the enfeebled respiratory and voice-sounds 
ordinarily detected in pneumothorax. Though such signs are 
most extraordinary, a large pulmonary cavity, if distended with air 
and partly filled with fluid, may yield succussion, metallic tinkling, 
and even the bell tympany of the coin test. 

Subphrenic pyopneumothorax, a, gas-containing abscess cavity 
situated between the diaphragm and the liver, counterfeits true 
pneumothorax, especially one circumscribed at the base of the chest. 
If the gaseous distention be excessive, the diaphragm is pushed up 
to a high level and the lung compressed, with the result that both 
physical signs and symptoms develop which intimately resemble 
those of an intrapleural effusion of air. In this differentiation the 
fluoroscope is most helpful, since it reveals, over a subphrenic pyo- 
pneumothorax, an abnormally high diaphragm shadow beneath the 
dome of which is a clear, luminous tract, indicative of air, and 
sharply contrasting with a horizontal zone of darkness corresponding 
to the underlying purulent collection. It is also of service to remem- 
ber that a subphrenic abscess is usually a sequel of gastric or intestinal 
perforation (as in gastric or duodenal ulcer), in consequence of 
which the subphrenic space, more commonly on the left side, becomes 
infected by material and distended by gas derived from the gastro- 
intestinal tract. 

In a rare emergency it is necessary to differentiate pneumothorax 
and diaphragmatic hernia, for in this grave accident the stomach 
and gut, ballooned with air, may protrude through a rent in the 
diaphragm into the thoracic cavity, thereby faithfully reproducing 
the physical conditions and signs of air within the pleural sac. Evi- 
dence in favor of hernia includes the detection of gastro-intestinal 
rumbling and sibilant noises over the lower thorax, as well as the 
important fact that should the hernial protrusion suddenly recede, 
as it sometimes does, both signs and symptoms will disappear coin- 
cidentally. A history of injury is no sure criterion, since it may be 
the factor of either condition. Congenital hernia of the diaphragm 
is occasionally encountered. 

A greatly dilated stomach, in so far as it can account for tympany, 
succussion sounds, tinkling noises, and embarrassed respiration, 
must be reckoned with as a possible mimic of left-sided pneumothorax. 



302 PHYSICAL DIAGNOSIS 

But the previous history of the two conditions is radically unlike, and 
in gastric dilatation there is no distinctive combination of signs, 
such as unilateral distention of the thorax, descent of the diaphragm, 
compression of the lung, and conspicuous displacement of the heart. 

PLEURAL NEOPLASMS 

Carcinoma. — The great majority of pleural neoplasms are 
secondary to carcinoma of the lung, which invades the pleural mem- 
branes by direct extension; less commonly the cancer arises by 
metastasis from a primary lesion of the lung, breast, gullet, or thyroid. 
Unilateral implication is the rule, affecting the right pleura somewhat 
more commonly than the left. Ordinarily, the cancerous lesions con- 
sist of multiple nodules, first appearing along the course of the lym- 
phatics and sometimes becoming so large as to excite active symptoms 
of intrathoracic pressure, to dislocate the mediastinum and its con- 
tents, and to bulge the chest-wall. Less commonly a diffusely dis- 
seminated type of growth is met with, the pleural membranes being 
densely infiltrated, welded together, and contracted, with the result 
that striking deformity of the chest ensues in the course of time. 
Cancer, as well as all other forms of pleural neoplasm, tends ulti- 
mately to excite inflammation of the pleura, generally with an effu- 
sion which in fully two-thirds of all cases is hemorrhagic. 

The physical signs of secondary cancer of the pleura are referable 
chiefly to the primary pulmonary lesion (see p. 267), and secondarily 
to the presence of either a plastic or an exudative pleurisy. If the 
latter exists, as is usually the case, an exploratory puncture should 
be made, with a view to finding in the aspirated fluid erythrocytes, 
free fat, cancerous elements, and a considerable number of mitotic 
cells. As a rule, the fluid also contains relatively few lymphocytes 
and many large vacuolated endothelial cells, commonly occurring in 
plaques. (See p. 54.) 

Aside from the important signs relating to the primary growth in 
the lung or some other locality, severe and stubborn pleural pain, 
cervical and axillary glandular enlargements, local chest deformity, 
and a cachectic appearance of the patient are to be regarded as 
important details of the clinical picture. The heart may be displaced 
either by effusion or by the growth, and dense adhesions may make 
the displacement permanent. 

Of primary carcinoma of the pleura, little need be said, for the 
disease is more often discovered by the pathologist than by the 
clinician. So long as the pleura alone is implicated the physical 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 303 

signs suggest merely a pleurisy, dry or effusive, for the constitutional 
evidences of malignant disease are not clearly denned. The develop- 
ment of metastases (i. e., in the lung, liver, or superficial lymphatics) 
is of distinct diagnostic aid, if such findings be reviewed in the light 
of the pleural manifestations. 

Sarcoma. — Sarcoma of the pleura is an exceedingly rare affection, 
and one impracticable to distinguish clinically from carcinoma, 
like which it is usually accompanied by hemorrhagic effusion, severe 
pain, deformity of the chest, and moderate, if any, cachexia. 
Invasion of neighboring and remote structures has been observed in 
the primary form, of which only about a dozen cases have been 
recorded. Secondary pleural sarcoma is also rarely met with, but 
the pleura appears to be more susceptible to sarcomatous than to 
cancerous implication by metastasis, in malignant disease primarily 
developing in other regions of the body. 

MEDIASTINITIS 

Simple acute mediastinitis is a rare affection, and its recogni- 
tion during life can only be hazarded. If the inflammation does 
not subside by resolution, its usual termination, either a fibrous over- 
growth or suppuration of the mediastinal tissues, may supervene, 
the clinical picture in each event being fairly definite. Though 
many cases must, unfortunately, be dubbed "idiopathic," in others 
a satisfactory cause is at hand, such as trauma and inflammation 
of the pericardium or of the mediastinal pleurae; abrupt suppression 
of the menses is a doubtful factor. 

Reliable physical signs are wanting in simple acute mediastinitis, 
the existence of which is suggested by the patient's history plus 
symptoms such as severe substernal and interscapular pain, per- 
sistent irritative cough, and moderate fever with rigors. 

Chronic mediastinitis accounts for more constant and active 
clinical findings than the acute form, since it consists not only of a 
mediastinal fibrosis, but also of more or less extensive pericardial 
inflammation and adhesion. Syphilis is a prominent factor in such 
cases, and intensive treatment with salvarsan is most helpful, even 
in the face of definite pressure symptoms. 

Following the classification of Thomas Harris, three patho- 
logic varieties are recognized: those in which there are both ex- 
ternal and internal adhesions of the pericardium, great increase 
of mediastinal fibrous tissue, and often caseation of the medias- 
tinal lymphatic glands (the indurative mediastino pericarditis of 



304 PHYSICAL DIAGNOSIS 

Kussmaul) ; those in which there are extensive external and internal 
adhesions of the pericardium, but little or no mediastinal fibrosis 
(the so-called external and internal pericarditis) ; and those in which 
there is decided mediastinal fibrosis attended by merely external 
pericardial adhesion (the true chronic mediastinitis) . 

Mediastinopericarditis is attended by great cardiac hypertrophy 
and dilatation, by chronic hepatic and renal congestion, and in 
some instances by proliferative peritonitis, perisplenitis, and a type 
of perihepatitis termed pericardiac pseudocirrhosis or Pick's dis- 
ease. Bronchitis, pleurisy, and pulmonary fibrosis are familiar 
associated conditions, and ascites, with or without general dropsy, 
is prone to occur, especially as the result of cardiohepatic lesions, 
peritonitis, and venous obstruction due to mediastinal pressure. 

The physical signs of chronic mediastinitis are referable mainly 
to the associated lesions of the heart and pericardium and to the 
sequelae arising therefrom. On inspection, there is seen a variable 
degree of thoracic immobility and dyspnea, perhaps with cyanosis, 
dropsy, and engorgement of the cervical and thoracic veins. Inspira- 
tory distention of the right external jugular vein is a suggestive though 
an inconstant sign: it indicates obstruction of the jugular return 
flow, due to compression of, or traction upon, the intrathoracic veins, 
and has been observed also in simple pericarditis, in pleurisy, and 
in mediastinal tumor. Palpation over the sternum, if roughly per- 
formed, may provoke lancinating pain. Of frequent occurrence 
is the paradoxic pulse, which weakens or completely disappears 
during inspiration, but this peculiarity is by no means distinctive 
of mediastinal fibrosis. (See p. 346.) Percussion shows, if the 
fibrosis be extensive, an abnormal area of dulness over and alongside 
the sternum, though such a finding is more often the result of the car- 
diac enlargement or of the mediastinal adenitis. On auscultation 
over the sternum one sometimes hears dry crackling mediastinal 
sounds and also the Eustace Smith hum (v. i.), while the rales of 
bronchitis and the friction-sounds of pericarditis and pleurisy gener- 
ally coexist. Evidences of cardiac dilatation and hypertrophy, of 
chronic adhesive pericarditis, and of hepatic (rarely, splenic) en- 
largement are also prominent details of the symptom-complex in 
many instances of chronic mediastinitis. 

Suppurative mediastinitis, due to the invasion of pyogenic cocci, 
occurs in consequence of trauma and of ulcerative diseases of the 
air-passages and gullet; it results also from the extension of septic 
lesions of the cervical fascia, the tracheobronchial glands, the lungs, 
and the pleurae; and it may be secondary to actinomycosis or to various 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 305 

acute infectious diseases, notably erysipelas, enteric fever, variola, 
and pyemia. The suppuration thus set up may occur as a wide- 
spread purulent infiltration' of the mediastinal tissues, or as one or 
more circumscribed abscesses. The former tends to run an acute 
and rapidly fatal course, attended by well-marked evidences of 
sepsis. The latter, if effectually walled in by a pyogenic membrane, 
often remains latent for a long period, and may even become absorbed 
or encapsulated; or the abscess may burrow through the mediastinal 
space and finally discharge through the line of least resistance — into 
the trachea, a bronchus, or the esophagus, through an intercostal 
space or downward along the spine, through the abdominal wall, 
or into one of the large blood-vessels. Tuberculous abscesses of 
the mediastinum are usually of limited extent, and do not give rise 
to severe systemic disturbances, save when secondary contamination 
with pyogenic microorganisms takes place. Cold abscess of the 
mediastinum can generally be traced to tuberculosis of the medias- 
tinal glands, or to caries of the spine or chondrosternal structures. 
It is the general belief that it most frequently affects the posterior 
space, while the other spaces suffer chiefly from the acute form (Hare) . 
The physical signs of mediastinal suppuration are notoriously 
untrustworthy, being quite negative in small deep-seated lesions. 
However, in a large abscess of the anterior or superior mediastinum 
inspection not infrequently detects a dusky, hot, fluctuating and 
sometimes pulsating swelling in the sternal region, while exceptionally 
actual pointing of the pus through the chest-wall is observed. The 
cardiac apex is enfeebled and dislocated in relation to the size and 
situation of the purulent collection. On palpation tenderness over 
the sternum is elicited, and the local peculiarities of the swelling are 
appreciated; in some instances there is a paradoxic pulse. Percus- 
sion may demonstrate undue upward and lateral extension of cardiac 
dulness, and also, in a large abscess of the posterior mediastinum, 
a dull area between the scapulae on either side of the spine. Evi- 
dences of mediastinal pressure (for a description of which see Medias- 
tinal Tumors, p. 309) arise, should the situation and the character 
of the abscess be such as to crowd the important vessels, nerves, and 
other organs of the mediastinum. Such symptoms are, as a rule, 
not so conspicuous in abscess as in mediastinal neoplasm. 



306 PHYSICAL DIAGNOSIS 

MEDIASTINAL LYMPHADENITIS 

Adenitis, either simple or suppurative, frequently affects the 
mediastinal lymphatic glands, of which there are three principal 
groups : those lying in the loose areolar tissue of the anterior space 
and also around the innominate veins, the aortic arch, and in front 
of the trachea; those situated along the esophagus and the aorta in 
the posterior space; and the bronchial group of the middle medias- 
tinum. Of these, the last named is of peculiar interest, owing to its 
intimate relation with the bronchi and, through afferents, with the 
lungs and pleurae. 

Simple lymphadenitis, with engorgement and edematous swelling 
of the glands, attends practically all bronchopulmonary inflamma- 
tions — bronchitis, bronchopneumonia, influenza— and occurs with 
especial frequency in the bronchitides of measles and pertussis. In 
the latter disease, indeed, the paroxysmal attacks of cough and 
dyspnea are interpreted by de Mussy as evidence of pressure by the 
enlarged lymph-nodes of the posterior mediastinum. Bronchial 
adenitis is an almost constant autopsy finding in pulmonary tuber- 
culosis. 

Suppurative lymphadenitis is generally of tuberculous origin, 
but it occasionally arises as the sequel of simple adenitis due 
to another factor. In some instances the suppuration is confined 
to the gland or group of glands primarily affected, and ultimately 
absorption of the pus and calcification of the lesion may take place; 
in other cases the pus burrows and finds an outlet, as by fistulation 
into a bronchus or into the esophagus; and in still others the infec- 
tion may extend to the lungs and pleurae, or mediastinal abscess may 
develop. In tuberculous adenitis the mediastinal focus of infection 
may account for the supervention of an acute miliary process 
and for phthisis, the former being due to the perforation of a 
vessel and the latter either to direct extension of the lesion or 
to the inspiration of tuberculous material which has eroded a 
channel into a bronchial tube. But pulmonary tuberculosis and 
glandular infection are by no means constant, even in long-standing 
tuberculous caseation of the lung — an example, Rist suggests, of 
allergy, like the acquired immunity of the buccal mucosa in phthis- 
ical subjects. 

The physical signs of mediastinal lymphadenitis are rarely definite 
enough to be of much value, save in an occasional case of extensive 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 307 

enlargement of the anterior mediastinal glands, in which abolished 
tactile fremitus, respiratory silence, and dulness are detected over 
and alongside the sternum; or the glandular masses may exagge- 
rate the bronchial sounds, combining bronchophony and intensified 
breath sounds with sternal dulness. In some instances the thoracic 
segment of the spine furnishes a group of most suggestive signs: 




Fig. 117. — Radiograph of mediastinal lymphadenitis. (Plate by Dr. VV. F. Manges.) 

tenderness from the second to the seventh spinous tip ; dulness over 
the fifth (normally resonant) ; and a patch of bronchial breathing 
and bronchophony at the level of the first. The writer is accus- 
tomed to place the same significance on the combination of hypo- 
resonance with maximum tactile resistance as on the association 



308 PHYSICAL DIAGNOSIS 

of hyperresonance with minimum tactile resistance in uncompli- 
cated adenopathies. It is assumed, to explain this apparent para- 
dox, that in the former instance the glandular mass exerts a dulling 
pressure, and that in the latter it conducts the predominant 
tracheal vibrations to the vertebral tips. 

It is frequently possible to demonstrate d'Espine's sign of 
tympany combined with exquisitely clear whispering pectoril- 
oquy over the upper thoracic vertebral spinous processes, and 
this sign is dependable as an early and most constant clue to 
adenopathies which, by structure and situation, act as effectual 
transmission paths for sounds generated within the large air- 
passages. 

Tracheobronchial tumors may compress the left innominate vein 
when the subject's head is stretched far backward, and thus pro- 
duce a venous hum audible over the manubrium — Eustace Smith's 
murmur. Paroxysmal cough, dyspnea, hoarseness, and dilatation 
of the venules upon the anterior surface of the thorax are pressure 
symptoms of decided importance. In children persistent dry 
cough, with negative surface signs, may be referable to enlargement 
of the lymph-nodes at the tracheal bifurcation, especially those 
situated below the right bronchus. Herbert French attributes the 
cough in such cases to irritation of the phrenic nerve. 

An #-ray examination usually reveals the presence of enlarged 
mediastinal glands, even at an early stage of their development 
(Fig. 117). The shadow cast by a group of hypertrophied bronchial 
glands suggests aortic aneurism, but an aneurismal shadow may 
show pulsation, and on inspection from various directions can 
generally be localized to some part of the aortic arch. In adult 
life the normal pulmonary radiograph ordinarily shows small isolated 
glandular shadows, for few persons reach maturity without at some 
time having been subject to a bronchopulmonary irritation whereby 
permanent adenoid enlargement is excited. In Fig. 70, a radio- 
graph of a perfectly normal thorax, the shadows alongside the 
mediastinal area indicate this wholly benign type of glandular 
enlargement, which is without pathologic significance. 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 309 
MEDIASTINAL NEOPLASMS 

Clinical Pathology. — Sarcoma and carcinoma are the most 
important types of malignant tumors affecting the mediastinal 
spaces, the former being decidedly the commoner of the two and 
more likely to be of primary origin. Primary sarcoma may arise 
from the thymus gland or its remains, or from the lymphatic glands, 
the pleuropulmonary structures, and the mediastinal tissues; second- 
ary tumors of this type are generally the sequel of an initial growth 
in some distant part. Primary carcinoma more commonly springs 
from the esophagus or the bronchopulmonary structures than from the 
thymus or connective tissue; secondary cancer of the mediastinum 
is prone to develop in the neighborhood of the primary tumor 
Among the rarer solid tumors of the mediastinum are included 
the simple lymphomata, and also growths of gummatous, fibrous, 
cartilaginous, osseous, • and teratomatous character. Of cystic 
tumors, hydatids and dermoids are examples exceptionally ob- 
served. The anterior mediastinum is the most common situation 
of malignant disease, and here is the selective site of sarcomatous 
lesions; for the posterior space carcinoma apparently has a pre- 
dilection. Not only does the mediastinal tissue become the seat of 
extensive malignancy, but its important organs as well as the neigh- 
boring structures also share in the change. Compression of the 
mediastinal vascular trunks, nerves, air-passages, and esophagus 
is produced, the pleurae, lungs, pericardium, and even the heart 
may become implicated, and in some instances the growth encroaches 
upon the neck, extends through the diaphragm, or presses against 
the anterior or the posterior chest-wall. Metastatic spread of the 
original growth is also likely to take place via the blood or the 
lymphatic vessels. 

For clinical study it is convenient to divide mediastinal tumors 
into two main groups : those of the anterior and superior mediastinal 
spaces, in which the physical signs overshadow the pressure phe- 
nomena; and those situated in the middle and posterior mediastina, 
in which the physical signs are subordinate to the pressure symptoms. 
It is perfectly obvious that this purely arbitrary classification is of 
limited applicability, since neoplasms tend progressively and erratic- 
ally to invade the different mediastinal compartments, thus giving 
rise to a medley of symptoms relating partly to this and partly to 
that space. Despite this, in order to trace the origin of such symp- 
toms, it is well to have a mental picture of these chief mediastinal 



310 PHYSICAL DIAGNOSIS 

compartments and of the effects produced upon their contents by the 
encroachment of morbid new-growths. 

Physical Signs. — Tumors of the Anterior and Superior Medias- 
tinum. — The principal signs of growths situated immediately beneath 
the sternum relate to the contour of the anterior chest-wall, to the 
consequences of compression or occlusion of the superior vena cava 
and the innominate veins, and to irritation of the superior laryngeal 
and sympathetic nerves. 

Inspection. — It is of some interest to note that the subject of a 
malignant tumor in this situation is anemic rather than character- 
istically cachectic, and that emaciation, though it does occur, is not 
usually conspicuous until the disease has almost run its course. 
Clubbing of the finger-tips generally develops in cases of long standing. 
Dyspnea is usually moderate, so long as the growth does not 
encroach far in a backward direction. As the result of persistent 
intrathoracic pressure the sternum finally gives way, and bulges out- 
ward to form a mound-like swelling (Fig. 118), or the growth may 
erode the chest-wall, appearing thereupon as a circumscribed node, 
of variable size, outline, and consistence, but tending ultimately 
to soften, to discolor, and to break down. Occlusion of the intra- 
thoracic venous trunks accounts for edema and for distention and 
tortuosity of the superficial veins of the face, neck, arms, and upper 
anterior chest- wall, bilateral phenomena of this sort indicating 
superior caval obstruction, and unilateral signs pointing to com- 
pression of an innominate vein or one of its tributaries. The illus- 
tration elsewhere shown (Fig. 51, p. 108) gives a good idea of the 
appearance of engorged superficial veins upon the surface of the 
body. Inequality of the pupils is not a frequent sign in growths af- 
fecting the anterior mediastinum, owing to the posterior position 
of the sympathetic nerve. Hoarseness and loss of voice, from com- 
pression of the inferior laryngeal, are, however, very common find- 
ings. 

Palpation. — Pressure over the sternum is painful to the patient, 
and palpation may detect a systolic pulsation over the tumor, the 
density of which ranges from stony hardness to soft edema. The 
lifting throb of a soft, overvascular tumor must be carefully dis- 
tinguished from the expansile pulsation of an aneurism. Tactile 
fremitus is usually abolished over the growth and its infiltrative 
extensions. In some instances the primary growth is palpable in 
the suprasternal notch, and secondary glandular enlargements appear 
in the neck and in the axillae. 

Percussion. — There is an area of dulness or of flatness correspond- 






DISEASES OF THE BRONCHOPULMONARY SYSTEM 311 

ing to the site of the tumor, in the immediate neighborhood of which 
hyperresonance is the rule. Abnormal modifications of the per- 
cussion sound are also likely to be found over other parts of the thorax, 
where associated pulmonary and pleural lesions exist. 

Auscultation. — Ordinarily, the respiratory murmur is suppressed 
over the tumor and exaggerated over the adjacent lung, but some- 
times the growth distinctly conducts, or even intensifies, the breath- 




Fig. 118. — Bulging of the thorax in a case of mediastinal neoplasm (Jefferson 

Hospital). 

sounds. Bronchial rales, pleural and pericardial friction-sounds, 
and systolic murmurs due to compression of the aorta and pulmonary 
artery are audible in certain cases. The cardiac sounds are fre- 
quently, though not invariably, obscure, muffled, and distant, par- 
ticularly at the base. 

Tumors of the Middle and Posterior M ediastinum .—In this situation 
growths, even of moderate size, cause signs referable mainly to com- 



312 PHYSICAL DIAGNOSIS 

pression of the vagus, the bronchi, and the gullet, while in some 
instances there are evidences of pressure upon the azygos veins and 
the inferior vena cava, as well as of extensive necrosis of the parts 
encroached upon. 

Inspection. — True cachexia, emaciation, asthenia, and fever are 
more common than in lesions of the anterior mediastinal space. 
The patient is constantly dyspneic and subject to alarming paroxysms 
of orthopnea, stridulous breathing, brassy cough, and dysphagia, 
due chiefly to vagus irritation, but in part to compression of the 
bronchopulmonary structures. Syncope, vomiting, symmetric cold- 
ness of the extremities, and disturbances of the cardiac rate, rhythm, 
and force also occur as the result of what Gowers terms "vagal 
attacks." The pulse, aside from its irregularity, is of feeble volume 
bilaterally, if the aorta be compressed, while differences in the 
force of the two radials is noticed in the event of pressure upon 
the innominate artery or upon the left subclavian. Edema of the 
lower extremities, ascites, and engorgement of the surface tribu- 
taries of the inferior vena cava are visual evidences of constriction 
of this great venous trunk. Inequality of the pupils, and some- 
times unilateral circumscribed flushing and perspiration, betoken 
irritation of the sympathetic cord. 

Palpation. — Considerable significance attaches to the sign noted 
by Graham Steell, who observed that the visible and palpable cardiac 
impulse covers an area almost coextensive with that of the entire 
heart, which, when encroached upon by a tumor of the posterior 
mediastinum, appears to thrust itself forward en masse with every 
systole. In other cases, where this diffuse impulse is not present, 
the apex-beat may merely be tilted outward and downward away 
from its normal site. 

Percussion. — Ordinarily, a tumor deep within the mediastinum is 
far beyond the reach of percussion, although should it extend back- 
ward against the posterior wall of the thorax, a patch of irregularly 
shaped dulness or flatness may be delimited in the interscapular 
region. It is not uncommon to find the basal flatness of intrapleural 
fluid, poured out usually as the result of an associated pleurisy, and 
exceptionally by fault of pressure stasis within an azygos vein. The 
percussion findings of pulmonary edema, excited by pressure upon 
the pulmonary veins, and of a distended right heart, due to pul- 
monary artery compression, are present in certain cases. 

Auscultation. — Of especial interest in connection with neoplasm of 
the middle and posterior mediastina are the physical signs of bronchial 
occlusion, partial or complete. (See p. 188.) Aside from this, 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 313 

evidences of recurrent laryngeal nerve implication and of secondary 
lesions of the lungs, pleurae, and pericardium should be given due 
attention. 

Diagnosis.— Usually it is not difficult to recognize mediastinal 
pressure, but it is quite another matter to prove that the pressure 
is due to malignant disease unless the case presents classic symptoms 




Fig. 119. — Radiograph of a mediastinal neoplasm. Lateral aspect, showing 
dense shadow in the anterior mediastinum, with infiltration of the sternum, and 
edema of the overlying chest- wall. (Plate by Dr. W. F. Manges.) 

and signs. The association of persistent dyspnea, dysphagia, sub- 
sternal and interscapular pain, venous obstruction, and nervous 
symptoms constitutes a syndrome scarcely to be misinterpreted, 
especially in the face of the physical signs of an intrathoracic tumor 
in a person who has steadily lost weight, failed in strength, and 
become anemic or cachectic. These signs having been obtained, in 



314 PHYSICAL DIAGNOSIS 

part or as a whole, it is perhaps justifiable to predict sarcoma when 
the lesion affects the anterior mediastinum, grows rapidly, attains 
a large size, and provokes striking local signs; and it seems also 
warranted to diagnose carcinoma when the growth occupies the pos- 
terior mediastinum, develops slowly, and is accompanied by few, 
if any, local manifestations. The radiograph is an invaluable aid 
in both the direct and the differential diagnosis, provided that its 
interpretation be sane and conservative. (See Figs. 119 and 120.) 




Fig. 120. — Radiograph of a mediastinal neoplasm. Anterior aspect, showing 
abnormal extension and density of the mediastinal shadow, with displacement of the 
heart. (Plate by Dr. W. F. Manges.) 



Aneurism of the aortic arch is the lesion most often confused with 
mediastinal tumor, and, indeed, it is sometimes quite impossible to 
make the antemortem differentiation. Diastolic shock, tracheal 
tugging, cardiac hypertrophy, true expansile pulsation, and an 
absence of glandular enlargement are in favor of aneurism, and a 
history of syphilis, unduly severe pain, and temporary amelioration 
of the symptoms after the use of the iodids make this inference the 
stronger. Furthermore, an aneurismal swelling generally occupies 
a higher level upon the anterior chest-wall than a growth pushing 
forward from the mediastinum, and the development of the former 



DISEASES OF THE BRONCHOPULMONARY SYSTEM 315 

is slower and the patient's lease on life longer, as a rule, than in 
malignant tumor. The fluoroscope reveals, in aneurism, a shadow 
that may clearly show expansile pulsation situated along the course 
of the aorta, while the shadow cast by a solid growth appears as an 
irregularly shaped extension of the mediastinal darkness which may 
or may not throb with cardiac systole. 

The differentiation of malignant disease versus gumma of the 
mediastinum has been referred to elsewhere. (See p. 247.) 



SECTION V 

EXAMINATION OF THE CARDIOVASCULAR 
SYSTEM 



CLINICAL ANATOMY 

The heart and its pericardial investment occupy the middle medi- 
astinal space behind the lower two-thirds of the sternum, the long 
axis of the organ being almost horizontal, and its greater part 
projecting to the left of the median line of the trunk. The normal 

adult's heart weighs approxi- 
mately from 9 to ii ounces 
(255 to 310 gm.), and shows 
maximum measurements of 
about 5 inches (12.5 cm.) in 
length, 3 J inches (8.75 cm.) 
in width, and 2\ inches (6.25 
cm.) in thickness. The ca- 
pacity of each ventricle is 
approximately 3 J ounces (100 
mils), according to Tigerstedt, 
and the auricles are capable 
of holding virtually the same 
volume of blood. The general 
shape of the heart is that of 
a blunt, somewhat flattened 
cone, having its base directed 
upward, its anterior convex 
surface placed upward and 
forward, and its compara- 
tively flat surface facing down- 
ward and backward. 
The pericardium consists of an outer fibrous and an inner serous 
layer, whereby the heart is completely enveloped, the viscus hanging 
free therein from its basal attachment to the great vessels; with the 

315 




Fig. 121. — Surface topography of the heart. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 



317 



fibrous layers of the latter the outer pericardium is continuous, while 
below it is anchored to the central tendon of the diaphragm. The 
inner pericardium is a closed sac formed by two serous layers: a 
parietal, which lines the fibrous pericardium, and a visceral, which 
covers the heart and is reflected therefrom along the great vessels. 
Like the heart, the pericardium is of a roughly conic shape, but unlike 
the cardiac cone whose base lies upward, the pericardial cone has 
its base directed downward. 

The Precordia (Fig. 122). 
— The term precordia, or pre- 
cordial region, designates that 
area of the anterior chest-wall 
which overlies the heart, and 
corresponds not only to the 
part of the organ directly im- 
pinging upon the inner surface 
of the thorax, but also to the 
portion overlapped by the 
pulmonary margins. The 
precordia, therefore, includes 
within its boundaries both the 
area of cardiac flatness and 
the area of cardiac dulness 
(q. v. i.). The relations of 
the heart to the chest-wall 
given below are those of the 
average normal adult, and 
more or less regional differ- 
ences must be expected in the 
individual case, owing to the influence of age, the state of the thoracic 
musculature and bony structures, and the development of the lungs. 

The base of the heart, consisting of the two auricles, lies in front 
of the descending thoracic aorta and the lower right pulmonary 
vein, being directed upward, backward, and to the right. It extends 
anteriorly from a point J inch (1.25 cm.) to the right of the sternum 
to a point 1 inch (2.5 cm.) to the left of this bone, at the level of the 
upper border of the third rib ; posteriorly, the base extends from the 
fifth to the eighth thoracic vertebra, inclusive. The right auricle 
lies beneath and somewhat external to the right half of the sternum, 
between the third and the sixth costal cartilages, but the greater 
part of the left auricle lies posteriorly, its appendage, beneath the 
second left intercostal space, being the only portion of this chamber 
to project toward the anterior surface of the thorax. The auriculo- 




Fig. 122. — The precordial and supracardiac 
areas. 



318 PHYSICAL DIAGNOSIS 

ventricular groove, separating the auricles from the ventricles, is 
indicated by a line extending from midsternum, at the level of the 
lower border of the third costal cartilage, to the sixth right chondro- 
sternal junction. 

The right border of the heart, formed by the right auricle, is 
represented by a line running from the right extremity of the base 
(upper border of the third rib, \ inch (1.25 cm.) from the sternum) 
to the sixth right chondrosternal articulation, and curving outward 
between these two points to attain a maximum convexity in the fourth 
intercostal space, which is crossed ij inches (3.75 cm.) from the 
midsternal line. 

The left border of the heart, corresponding to the left ventricle, 
follows a line curving slightly outward from the left extremity of the 
base (upper border of the third rib, 1 inch (2.5 cm.) from the sternum) 
to the anatomic cardiac apex (q. v. i), situated in the fifth left inter- 
costal space, in the midclavicular line. From somewhat to the right 
of this point the interventricular groove, dividing the ventricles, runs 
anteriorly upward to the third left chondrosternal junction. 

The lower border of the heart, formed almost entirely by the 
right ventricle, though to a slight extent by the left ventricle, is mapped 
out by drawing a line from the apex to the lower extremity of the 
right border (sixth right chondrosternal articulation), which line 
crosses the xiphoid cartilage just below its sternal attachment. 

The cardiac valves and orifices are included within the boun- 
daries of a flattened circle, extending obliquely across the body of 
the sternum from the third left to the sixth right chondrosternal 
articulation (Fig. 134). From above downward the valves lie in the 
following order: pulmonic, at the upper border of the third left 
chondrosternal joint; aortic, beneath the left half of the sternum, at 
the lower border of the third costal cartilage; mitral, beneath the 
left half of the sternum, at the level of the fourth costal cartilage; 
and tricuspid, extending from midsternum, at the level of the fourth 
costal cartilage, to the fifth right chondrosternal junction. The 
foregoing landmarks refer only to the anatomic sites of the valves, 
the individual tones of which and the murmurs pertaining thereto 
are most clearly audible over that area of the thorax where the valve's 
chamber approaches closest to the surface. These sites, known as 
"valve areas," or " auscultatory areas." are referred to in connection 
with auscultation of the heart. (See p 364.) 

The Supracardiac Vascular Area (Fig. 122). — The great blood- 
vessels arising from the ba^e of the heart lie within a rectangular 
area extending from the clavicles to the cardiac base line, and bounded 
on either side by vertical lines projected upward from the latter's 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 319 

right and left extremities. This space, then, overlies the superior 
vena cava, the aortic arch, the innominate artery, and the innominate 
veins. The superior vena cava extends from the confluence of the 
innominate veins, at the right sternoclavicular joint, to its outlet 
into the right auricle, at the third chondrosternal articulation, the 
course of the vessel between these two points lying beneath and 
somewhat external to the right sternal edge. The ascending aorta 
lies behind the sternum between the third left chondrosternal junction 
and the second right costal (or aortic) cartilage. At this point the 
aortic arch commences, and runs thence obliquely upward and back- 
ward toward the fourth thoracic vertebra, where it becomes con- 
tinuous with the descending thoracic aorta; the highest point of the 
aortic arch in the median line usually lies 1 inch (2.5 cm.) below the 
suprasternal notch, or at about the center of the manubrium. The 
pulmonary artery runs along the left sternal border beneath the 
second intercostal space and the second costal cartilage. The 
innominate artery, arising from the upper aspect of the aortic arch, 
runs obliquely upward to the right sternoclavicular junction, where 
it divides into the right subclavian and common cartoid arteries; 
on the left side these two vessels spring from the aortic arch between 
its middle and posterior extremity, the common carotid coursing 
obliquely, and the subclavian running almost vertically, upward 
into the neck. Of the two innominate veins, the right lies under 
the inner extremity of the right clavicle, and the left, beneath the 
upper portion of the manubrium. 

MECHANISM OF THE CIRCULATION 

The Cardiac Cycle. — This term refers to the series of events that 
attend each beat of the heart, whose cycle, therefore, comprises the 
systole or contraction of the auricles, the systole or contraction of the 
ventricles, and the period of diastole or relaxation and passivity 
of both auricles and ventricles. In a clinical sense, the words systole 
and diastole, when used without a qualifying adjective, mean con- 
traction and relaxation, respectively, of the ventricles. Normally, 
the systolic and diastolic phases on the right and left sides of the 
heart are precisely synchronous, the auricles contracting and relaxing 
at exactly the same moment, and the ventricles doing likewise. The 
entire cardiac cycle lasts 0.8 second, of which 0.1 second is occupied 
by the auricular systole, 0.3 second by the ventricular systole, and 
0.4 second by the diastole of all four chambers. Acceleration of the 
cardiac action, which abbreviates each of these cyclic phases, especially 
affects the diastolic. The component parts of the cardiac cycle 



3 20 



PHYSICAL DIAGNOSIS 



and their relation to the cardiac sounds and impulses are graphic- 
ally shown by the accompanying diagram (Fig. 123). 

The origin and maintenance of the cardiac cycle are best explained 
by assuming an inherent automatic rhythmicity of the myocardium, 
whereby orderly waves of contraction are generated at the venous 
end of the heart and are conducted thence throughout the organ 
by its musculature. This myogenic theory of the heart-beat attrib- 
utes to the cardiac muscular fibers the functions of " rhythmicity, 
excitability, contractility, conductivity, and tonicity" (Gaskill), 



p — >7recorJial Impulse .< — 




%-O.Uec. 



Fig. 12.3. — The events of the normal cardiac cycle. 



whereby the heart can beat independently of nerve control, the vagus 
and the sympathetic nerves merely regulating the force and the rate 
of the contractions. These are probably excited directly by certain 
inner stimuli due to the action of ionized salts (especially sodium, 
calcium, and potassium ions) in solution in the juices of the tissues. 

Opposed to the foregoing, the neurogenic theory of the heart-beat 
takes for granted that inner stimuli exciting cardiac contractions arise 
in the intrinsic nerve-cells of the auriculovenous area, whence impulses 
travel, via nerve paths, to subsidiary nerve-centers, through which the 
auricular and ventricular contractions are activated. This theory, 
which is unsupported by positive proof, burdens the intrinsic cardiac 
nerves with the spontaneity, the orderly sequence, and the harmonious 
relations of the several events of the cardiac cycle. 

The Cardiac Movements. — The earliest phase of the cardiac 
cycle is a quivering contractile movement at the mouths of the venae 
cavae and pulmonary veins, presumably initiated at the caval orifice 
in a minute node of primitive tissue representing the remains of the 






EXAMINATION OF THE CARDIOVASCULAR SYSTEM 32 1 

sinus venosus — the sino-auricular node of Keith and Flack. Sys- 
tole of the auricles immediately follows, 1 as the peristaltic wave 
extends downward through the musculature of these chambers, 
to the auriculoventricular bundle of His, which arises from a node 
in the wall of the right auricle (Tawara's auriculoventricular node) 
and is distributed through the ventricular musculature. After a 
momentary delay as it crosses the auriculoventricular bridge of mus- 
cle, the contraction traverses the ventricles, first downward through 
the wall toward the apex, and finally inward to terminate in the pap- 
illary muscles. 

The recent work of Kent suggests that cardiac impulses also may 
arise spontaneously in a mass of nodal tissue situated in the lateral 
aspect of the right auricle, and pass thence downward into the 
ventricles along a muscular channel connecting the upper and the 
lower chambers of the heart. In the event of the destruction of 
His' bundle it is possible that impulses are conducted to the 
ventricle along this right lateral bridge of Kent. 

The ventricular systole thus excited is followed by auricular 
diastole, which begins as the earliest waves of contraction pass 
through the ventricles. The latter, after having ejected their 
contents into the arterial system, relax in diastole, and this final 
phase of the cycle is succeeded by a relatively long resting period 
which ushers in the next series of contractions at the auricular out- 
lets of the great veins. During its contraction the heart twists for- 
ward upon its long axis from left to right, the ventricles harden, 
shorten, and thicken, and the apex, now pointed, tilts upward and to 
the right; the auricles diminish in size and recede, while the aorta 
and pulmonary artery distend and lengthen. With diastole the 
heart rotates backward and to the left, the ventricles become 
flaccid and globular, the apex becomes rounded and shifts down- 
ward and to the left; the auricles distend and protrude, and the 
aorta and pulmonary artery collapse and shorten. 2 

With auricular systole the blood in the auricles is forced through 
the auriculoventricular orifices into the relaxed ventricles. Reflux 
into the venae cavae and pulmonary veins (which are not guarded by 

^achmann has proved that the auricular contractions are not precisely- 
synchronous, the right auricle contracting an appreciable time (0.013 second) 
before the left. 

2 "Williams and James have proved, by electrocardiographic tracings, that 
there may be a true reversal of the cardiac action, the ventricles contracting 
before the auricles and the impulses initiated in the lower chambers passing up 
His' bundle into the auricular muscle. Such a condition is referable to a 
prevailing dominance of the intrinsic ventricular rhythm over the normal sinus 
rhythm whereby the feebler stimuli of the latter are overshadowed. 



322 PHYSICAL DIAGNOSIS 

valves at their outlets) is prevented by several factors : chiefly by the 
low intra-auricular pressure, 1 but partly by the constriction of the 
venous orifices by the contraction of their muscular coats, as well as 
by the free outlet afforded the blood-stream by the widely dilated 
mitral and tricuspid openings. 

The ventricular diastole, which coincides with the entire systole of 
the auricles and with the last part of their diastole, is due mainly to 
the inherent resiliency of these chambers. During this period the 
ventricles .fill with blood, which gradually floats up the mitral and 
tricuspid curtains, so that they close, by the end of diastole, their 
respective orifices. Meanwhile the semilunar valves, kept tightly 
closed by the high arterial pressure, prevent leakage of blood from 
the aorta and pulmonary artery. 

The ventricular systole now occurs, and the blood contained in the 
ventricles is pumped forward into the aorta and pulmonary artery, 
whose semilunar cusps are simultaneously forced open as soon as the 
pressure in the ventricles exceeds that in the arteries, this change of 
tension taking place immediately after the ventricles commence to 
contract. Regurgitation into the auricles cannot occur because the 
mitral and tricuspid valves, already approximated by the pressure 
of the blood distending the ventricles, are kept tightly closed by the 
impact of the reflux current excited by the contraction of these 
chambers. The contraction of the papillary muscles not only aids 
in perfectly apposing the margins of the cusps, but also prevents 
the eversion of the valves into the auricles. The aortic blood-column 
courses through all parts of the body, after which it is returned, by 
the venae cavae, to the right auricle, this complete circuit from the 
left ventricle to the right auricle being known as the systemic or 
greater circulation. The blood in the pulmonary artery is propelled 
through the lungs, whence it flows back, oxygenated, through the 
pulmonary veins, into the left auricle, this short circuit being termed 
the pulmonary or lesser circulation. 

During auricular diastole the blood returns from these two circuits, 
for at this period of the heart's cycle the pressure in the venae cavae 
and pulmonary veins exceeds that in the auricles. The latter are 
distended by the volume of their contained blood, aided to some 
extent by the elastic traction exerted by the lungs, the auriculo- 
ventricular openings meanwhile remaining closed. 

Arterial Tension. — The term blood-pressure designates the 
mural tension of the blood-vessels exerted by the lateral and radial 

x The pressure in the ventricles, which at this -time are in diastole, is also 
much lower than in the veins, being so low, indeed, that it is believed to exert 
a so-called "suction action" upon the entering blood-stream. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 323 

force of the circulating blood-stream, the degree of this pressure 
varying in different parts of the vascular path, according to their 
proximity to the heart. In this central pump the pressure reaches 
the maximum, in the arteries it diminishes, in the capillaries it 
becomes still lower, and in the veins it falls to a minimum; in conse- 
quence of these differences the blood-stream courses uninterruptedly 
through the body from its ventricular high-pressure outlets at the 
aortic and pulmonary orifices to its auricular low-pressure inlets 
at the mouths of the cavae and pulmonary veins. In the venous 
channels the blood is impelled heartward by three factors: the 
initial cardiac force, the aspiration action of the heart and thorax, 
and the pressure exerted by the body musculature upon the valvular 
parts of the veins. 

Arterial tension is maintained by the pumping force of the ven- 
tricles and by the peripheral resistance, and so long as these two factors 
work so as to equalize the vascular outflow and inflow of blood, the 
normal equilibrium of pressure remains undisturbed. The vaso- 
motor system of nerves, aside from regulating the distribution of the 
blood-mass, is a most important factor in determining the height of 
the blood-pressure. Stimulation of the vasoconstrictors contracts 
the peripheral arterioles, and in so doing increases peripheral resis- 
tance, thereby raising arterial tension; paralysis or extreme exhaustion 
of the constrictors has an opposite effect. Stimulation of the vaso- 
dilator nerves, by dilating the arteriolar caliber and diminishing 
peripheral resistance, lowers arterial tension — a condition, it may 
be added, much more readily induced than increased tension, owing 
to the relatively greater susceptibility of the vasodilators to stimulating 
influences. 

The acme of hypertension develops when a powerful, overacting 
heart impels the blood-column against the undue resistance excited 
by tight vasomotor constriction, while the lowest degree of tension 
is found when a feeble, toneless heart is linked with the minimized 
resistance resulting from extreme vasomotor dilatation. 

INSPECTION AND PALPATION 

It is convenient to discuss inspection and palpation of the cardio- 
vascular apparatus together, rather than to make an artificial division 
of this dual method of research. The examiner should invariably 
preface his investigation of the precordial region by a careful inspec- 
tion of the subject's facies, skin, and subcutaneous tissues, general 
nutrition, thoracic configuration, and respiratory movements. This 



324 PHYSICAL DIAGNOSIS 

preliminary inquiry, the details of which have been considered 
elsewhere (p. 79 et seq.), is primarily directed toward the discovery 
of the more general objective symptoms of heart disease — pallor, 
cyanosis, and icterus; clubbing of the fingers, coldness of the extremi- 
ties, venous tortuosity, and edema; and polypnea, dyspnea, and 
other forms of respiratory distress. Advanced disease of the mitral 
valve, for example, is suggested at first glance by the pasty, puffy, 
dusky face, the clubbed, cold fingers, and the panting respiration 
of the subject; coronary artery obstruction and aortic arterioscle- 
rosis by a dull, ashen pallor — the "leaden overcast'' of Sansom; 
while the association of violent arterial throbbing, urgent dysp- 
nea, and an apprehensive fades, by turn pallid and flushed, spells 
Corrigan's disease to the trained eye. 

More definite information relating to the condition of the heart 
and blood-vessels is obtained by further inquiry, which should in- 
clude the study of the precordial contour, the apex-beat, the presence 
or absence of unnatural pulsation and retraction, and the questions 
of thrills and friction fremitus. In looking for obscure pulsations and 
irregularities of contour it often proves most helpful to resort to 
K. H. BealPs device of drawing with a skin pencil, upon the sur- 
face under investigation, a plaid figure composed of one-inch 
(2.5 cm.) squares, whose fines become obviously distorted by surface 
movements and irregularities not otherwise perceptible. 

Semirecumbency is the best position for the subject to assume 
during routine inspection and palpation of the heart and great 
vessels, but it is frequently advisable to test the effect of gravity upon 
certain signs (pulsations, thrills, and tactile fremitus), by employing 
alternately the upright and the recumbent positions. 

The influence of bodily posture upon cardiac physical signs has 
been succinctly summed up by William Gordon, who states that a 
change from the erect to the recumbent position: (a) raises and 
narrows the normal cardiac dulness; (b) greatly narrows the dul- 
ness of an enlarged heart; (c) dulls the first, and sharpens the 
second, cardiac sound; (d) exaggerates an accentuated pulmonic 
second sound and a reduplicated second sound; (e) intensifies 
hemic, mitral and tricuspid regurgitant, and aortic stenotic mur- 
murs; (/) enfeebles the venous hum and the mitral stenotic bruit; 
and (g) leaves unaltered the murmur of aortic regurgitation. 

The Precordial Contour. — Bulging of the precordia, disturbing 
the normal bilateral symmetry of the anterior chest-wall, is much 
more likely to occur in children than in adults, in consequence of 
the greater resiliency of the parietes during immaturity, and their 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 325 

readiness to yield to intrathoracic pressure. (See Fig. 40, p. 91.) 
A prominent precordial region suggests pericardial. effusion, enlarged 
heart, circumscribed pleural effusion, mediastinal tumor, or aneurism 
of the aortic arch, whereby the surface of the chest is mechanically, 
if not erosively, made to protrude outward. Less commonly, the 
deformity is traceable to some factor such as rickets, anterolateral 
spinal curvature, or inflammatory thickening of the surface structures. 

Precordial flattening or depression, either general or local, may 
signify pericardial adhesions, in which event the change usually is 
best defined in the lower left parasternal area. Flattening of the 
precordia is also referable to left-sided pleural adhesions and to 
fibroid retraction of the left lung. The depression of the lower 
sternal region typical of the "funnel chest, " the mesial sternal furrow 
of the "gutter chest," and the sunken breast-bone of the "boat- 
shaped thorax" have been referred to under Examination of the 
Thorax. (See p. 85.) 

The Apex-beat. — In the healthy adult the apex-beat of the heart 
is recognized as a rhythmic local pulsation in the fifth left intercostal 
space, half an inch (1.25 cm.) internal to the midclavicular line, or 
3§ inches (8.75 cm.) external to the midsternal line; it corresponds, 
in other words, to the lowermost outermost circumscribed pulsa- 
tion recognizable upon the left anterior or anterolateral surface of 
the thorax. 

In young children the apex is commonly observed in the fourth 
interspace, and as far outward as the left midclavicular line; in 
short-chested subjects it may be similarly elevated; and in persons 
of advanced age and in those having a long chest it may beat at an 
unnaturally low level. The word bathycardia has been proposed 
by E. J. Janeway to signify a low position of the heart due to physio- 
logic causes. 

The apical pulsation is systolic in time, being synchronous 
with ventricular systole, and is ordinarily restricted to an area not 
more than an inch (2.5 cm.) in diameter. In health the right ven- 
tricle is to be regarded as the clinical apex of the heart, and to the 
systolic impact of this chamber against the inner thoracic wall the 
surface pulsation is due; the left ventricle, which is the anatomic apex 
of the heart, does not, unless enlarged, directly produce an appre- 
ciable pulsation of the overlying parietes. Usually the apex-beat 
can be both seen and felt, but it is by no means rare to find it invisi- 
ble, though it is distinctly palpable as a gentle, pushing thrust appreci- 
ated by the finger-tip applied to the apex region. Deep inspiration 
slightly depresses, and forced expiration elevates, the site of the apex, 
which also shifts horizontally when the subject turns from dorsal to 



326 PHYSICAL DIAGNOSIS 

lateral recumbency, the deflection amounting to an inch or two 
toward the left when left lateral decubitus is assumed. Postural 
mobility of the apex, which is greater in adults than in children, 
is especially apparent in subjects of cardiovascular disease. 

Having identified the apex-beat, it is necessary to learn whether 
the impulse is situated normally or displaced, whether its force is 
exaggerated or enfeebled, and whether the area of pulsation is 
diminished or extended. These points are decided by combined 
inspection and palpation of the precordial region. 

Displacement of the Apex-beat. — Of the numerous factors of apical 
displacement, the most important relate to enlargement of the heart 
by hypertrophy and dilatation, to dislocation of the organ by intra- 
thoracic traction or pressure and by ascent of the diaphragm, and 
to the collection of fluid within the pericardial sac. Aside from these 
causes, the effect of thoracic deformities and of visceral transposition 
on the site of the apex-beat is also to be recalled. 

Upward apical displacement may indicate unduly great subphrenic 
pressure, in consequence of which the diaphragm, and with it the 
heart, rises to a high level, as in ascites, meteorism, gastric distention, 
and abdominal tumor; diaphragmatic hernia also may elevate the 
heart's impulse. Upward displacement, with more or less deviation 
of the apex to the left, occurs from effusion of fluid or of gas in the 
right pleural sac, adhesions of the left pleura and fibrosis of the 
corresponding lung, large pericardial effusion, and mediastinal 
neoplasm. A heart that has undergone considerable atrophy 
obviously is likely to pulsate at too high a site. 

Downward apical displacement ordinarily is referable to pressure 
exerted by hypertrophic emphysema; less commonly the weight of an 
aortic aneurism or of a mediastinal tumor depresses the apex; or it 
may be dragged downward by an enlarged liver or by some form of 
visceral ptosis. 

Right lateral apical displacement is generally attributable to such 
lesions as right-sided pulmonary fibrosis and pleuropericardial 
adhesions; to collapse of the right lung; and to the pressure of a left- 
sided pleural effusion or pulmonary consolidation. In congenital 
transposition of the viscera the apex-beat is to be looked for at a 
point in the fifth right interspace, near the midclavicular line — a 
condition of dextrocardia giving the so-called "mirror image" of the 
precordial and other regions. 

Left lateral apical displacement, if practically horizontal, is espe- 
cially significant of dilated hypertrophy of the right ventricle, whose 
strong epigastric and parasternal pulsations must not be mistaken 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 327 

for its actual apical impulse. The apex beats to the left of, and be- 
low, its normal situation in dilated hypertrophy of the left ventricle. 

The character of the apex-beat as to force, extent, and rhythm 
varies both in health and in disease, so that should such deviations 
from normal be found, it is necessary first to determine if they are 
physiologic or pathologic, and, if the latter, to discover the lesion, 
cardiac or extracardiac, upon wh'ch they depend. In judging the 
force of the apex-beat, allowance is to be made for the facts that a 
thin chest-wall magnifies, and a thick chest-wall minimizes, the 
impulse; and that should the impact of the ventricle be directed 
against a rib rather than an interspace, the apex-beat naturally will 
be indefinable by inspection and palpation. The apex-beat may 
also be absent in an individual whose thorax is so deep that the 
heart fails to impinge against the inner thoracic wall. 

Simple exaggeration of the force of the apical impulse may be due 
to nervous excitement, overexercise, indigestion, anemia, and the 
overuse of tobacco, coffee, tea, and alcohol. The "fluttering" 
of the heart complained of by the neurotic woman, and the precordial 
throbbing of the indiscreet coffee-drinker and smoker, are familiar 
illustrations of this type of apex overaction. It may accompany 
acute myocarditis, valvular disease, and left ventricular hypertrophy — 
in the last-named lesion the impact is not only forcibly heaving, but 
diffuse and displaced downward and to the left. Forcible throbbing 
of the apex attends the initial stages of many acute febrile dis- 
eases, and is seen in apoplexy. An apparently exaggerated apex- 
beat may be due to retraction of the left lung, w 7 hereby the heart 
is uncovered and hence pulsates against the chest-wall more forcibly 
and more extensively than in health. 

An enfeebled or absent apex-beat should always arouse one's sus- 
picion of cardiac dilatation, the relaxed ventricle either quite oblitera- 
ting the impulse, or rendering it feeble, undulatory, and of a distinc- 
tively " slapping" character. The slow, deliberate systole of the 
left ventricle commonly associated with aortic stenosis may be so 
forceless as to give rise to no appreciable impulse in the region of the 
apex. Pericardial effusion, emphysema, and mediastinopericardial 
adhesions also are capable of weakening or negativing the apical 
beat — pericardial effusion, by interposing a barrier of fluid between 
the heart and the thoracic wall; emphysema, by hemming in the 
whole anterior surface of the heart with a mass of overdistended 
lung tissue; and mediastinopericardial adhesions, by mechanically 
restricting the heart's excursions by the contraction of the fibrous 
bands by which the organ is anchored. Advanced myocarditis, 
myocardial degeneration, cardiac atrophy, and systemic shock and 



328 PHYSICAL DIAGNOSIS 

debility materially lessen the force of the apex-beat. Exceptionally, 
every trace of the precordial impulse is obliterated by either a 
neoplasm or an inflammatory lesion of the anterior mediastinum, 
whereby the heart is pushed backward and its throbs are com- 
pletely damped. 

The cardiogram of the apex-beat (Fig. 124; cf. Fig. 14) may 
show unnatural deviations that serve, within reasonable limits, as 
criteria of disturbances affecting the rate, force, and rhythm of the 




Fig. 124. — Normal cardiogram of trie apex-beat: a, Auricular systole; a-b, 
upstroke (systole); b, apex; b-c-d, systolic plateau (cardiac impact); d-e, downstroke 
(diastole); d, aortic valve closure; e-f-a, ventricular filling. (Tracing by Dr. G. 
Bachmann.) 

heart, more especially when interpreted in the light of simultaneous 
tracings of the radial and jugular pulsations. The cardiographic 
upstroke is, unfortunately, no certain index to the force of the ven- 
tricular systole, since a sudden, sharp impact of the heart, though 
the actual force be subnormal, may produce quite as high a rise as 
that due to a powerful contraction. Uneven spacing of the upstroke 
intervals, if instrumental defects can be excluded, means ventricular 
arhythmia. The apex, if sharply acute, denotes rapid emptying of 
the ventricle, as the result, for example, of the double ventricular 
outlet established by fault of a mitral insufficiency; an obtuse, blunt 
apex indicates an opposite state of things, as in aortic stenosis. The 
systolic plateau corresponds in length to the duration of ventricular 
systole, and an unduly broad and horizontal wave in this situation 
suggests the deliberate systoles which accompany many cases of 
aortic stenosis. The downstroke, being related to diastole, follows 
a course the obliquity of which increases in correspondence with the 
prolongation of this phase. The diastolic rise ascends as a short, 
steep curve when diastole is sharp and sudden, but mounts gradually 
upward when the diastolic relaxation is prolonged. Vertical oscilla- 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 329 



tions of the base line, it should be also noted, are explained chiefly 
by disturbances in the waves of the diastolic rise and fall between 
the systolic plateau and upstroke. 

Abnormal Areas of Pulsation (Fig. 125). — Apart from pulsations 
directly referable to the apical thrust, those occurring in other parts 
of the precordia and in regions of the thorax adjacent thereto remain 
to be identified and interpreted in an etiologic light. Such anomalies 



Jugular 




Right ventricle 



Innominate; aorta 
Phantom aneurism of 
axillary artery 

Conus arteriosus 

Pulsating pleurisy 

Right ventricle 
Aorta; right ventricle 
Left ventricle 
Aorta 



^^ Cardiac "^ 
(~^\ Vascular V Pulsations 
(jQ) Visceral J 
Fig. 125. — Areas of abnormal pulsation. 

arise chiefly from lesions of the heart and large vascular channels, 
but they may also be due in many instances to a conduction of the 
normal cardiac and arterial impact by the medium of neighboring 
morbid structures. Like the apex-beat, these pulsations are often 
both visible and palpable, though some are palpable only; unlike 
the apex-beat, an extra-apical pulsation may have a distinctly expan- 
sile character and may be found over a local tumor upon the surface 
of the chest. Pulsations of cardiac origin are typically systolic in 
time, but those of arterial and venous nature vary in time-incidence 



330 PHYSICAL DIAGNOSIS 

according to the mechanism whereby they are produced. The 
neck, the area corresponding to the base of the heart, the precordia 
and its vicinity, the epigastrium, and the region of the liver all should 
be examined for evidences of abnormal throbbing, whose rhythm 
is determined by comparison with the apex-beat. 

Pulsations on either side of the neck may originate in the carotid 
artery or in the jugular vein. If carotid, it is recognized as a systolic 
throbbing along the course of the vessel from the sternoclavicular 
articulation to a midpoint between the angle of the jaw and the 
mastoid process. Pulsation in this site is due to much the same 
factors that account for a tumultuous apex-beat — neurotic influ- 
ences, overexertion, and the abuse of tobacco and other heart irri- 
tants. Carotid pulsation is especially significant of left ventricular 
hypertrophy, with or without aortic leakage; of aneurism of the 
aortic arch; of exophthalmic goiter; of advanced arterial sclerosis; 
of cerebral hemorrhage; and of high-grade anemia. In rare in- 
stances the cause has been found to be an obliterative endarteritis 
of the descending portion of the aortic arch. Local expansile pul- 
sation of a common or an external carotid artery may be due to a 
small aneurysmal dilatation of the vessel. 

Pulsation under the outer half of the left clavicle occurs as a tem- 
porary intermittent sign in local dilatation of the axillary artery 
(Samuel West), and may be accompanied by circumscribed swell- 
ing, venous engorgement, thrill, and murmur. This syndrome, 
while highly suggestive of aneurysm, is readily differentiated there- 
from by its transient, evanescent character. 

Pulsation of the jugular veins, which is always more marked on 
the right side, is recognized as a throbbing along the course of these 
vessels upward over the clavicular belly of the sternocleidomastoid 
muscles. It is of the greatest importance to determine whether 
these pulsations are systolic, presystolic, or both. Systolic jugular 
pulsation is almost proof positive of tricuspid valve leakage, and 
indicates a ventricular, or positive type of venous pulse; presystolic 
jugular pulsation is not necessarily pathologic, and means an auric- 
ular, or negative, variety of venous pulse. Very exceptionally, it 
is possible to assign a factor other than tricuspid leakage to a systolic 
venous pulse, as, for example, aneurism implicating the superior 
cava, and also mitral regurgitation plus patent foramen ovale, both 
of which defects favor transmission of the ventricular impact through 
the venous columns emptying into the right heart. The differentia- 
tion and clinical significance of these two kinds of jugular pulsation 
are considered under the Venous Pulse. (See p. 346.) 

Ordinarily, the venous pulse is observed only in the jugulars, 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 33 1 

but in extreme cases it may penetrate their smaller surface tribu- 
taries and extend to other extremital veins. The palpable hepatic 
pulse, described below, shows the extent to which the ventricular 
beats sometimes regurgitate through the veins. 

Diastolic collapse of the jugulars {Friedreich's sign) occurs with 
frequency in chronic adhesive pericarditis; it has been attributed 
to a sudden emptying of these veins at the time of diastole, which 
allows the chest-wall, tightly drawn in by adhesions during systole, 
suddenly to relax and expand, and thus to exert an aspiratory action. 
Collapse of a jugular vein, if permanent despite pressure centrally 
applied, is significant of thrombosis of the lateral sinus. 

Pulsation in the episternal notch may not be abnormal in the 
emaciated and in the aged, and it also may arise as the result of neu- 
roses, anemia, and indulgence in stimulants. Other causes of a systolic 
pulsation in this area are dilatation of the transverse portion of the 
aortic arch, usually aneurismal; aneurism of the innominate artery; 
and exposure of the right subclavian artery by a contracted lung 
or conduction of its pulsation by a consolidated lung of the corres- 
ponding side. The existence of cervical ribs, and anomalies in the 
size and distribution of the vessels at the root of the neck are also 
among the possible causes of a systolic throb in this region. 

Pulsation at or near the base of the heart, if not due simply to violent 
cardiac overaction, may mean aneurism of the aortic arch, or dilata- 
tion of the arch in consequence of atheroma or of Corrigan's dis- 
ease. Systolic throbbing in the first or second right intercostal spaces 
near the sternal border is produced by aneurism of the ascending 
portion of the aortic arch; over the angle of Louis, at the level of the 
second rib, by aneurism of the transverse portion; and in the second 
or third left interspaces, by aneurism of the descending portion. 
Aneurismal throbbing in these sites, when typical, is attended by a 
distinct diastolic shock, and should it occur over a circumscribed 
bulging of the chest wall, has an expansile character. The impulse 
of the conus arteriosus of the right ventricle may account for a 
systolic pulsation near the left sternal edge as high up as the second 
interspace. Diastolic pulsation in the second left interspace near 
the sternal border is a common early sign of incipient pericarditis. 
Pulsation between the right sternal and midclavicular lines and 
between the second and fourth interspaces is sometimes due to 
displacement of the heart by the traction of a fibroid right lung, or 
by the pressure of left-sided pleural effusion, pneumothorax, or 
neoplasm. 

Pulsation in the precordial area in the third, fourth, or fifth inter- 
spaces at the right sternal border may be caused by cardiac dislocation 



332 PHYSICAL DIAGNOSIS 

from any of the factors just mentioned, but it also commonly results 
from right auricular dilatation. An hypertrophied and dilated right 
ventricle may be the factor of throbbing immediately alongside the 
left sternal border, between the third and sixth interspaces inclusive. 
Pulsating pleurisy, usually purulent, sometimes produces a throbbing 
or an undulation of one or several interspaces, almost invariably 
on the left side, between the second and sixth ribs, and between the 
left border of the precordia and the axilla. 

Pulsation in the epigastrium depends upon a number of different 
factors, referable in the main to the heart, the gut, and the viscera 
of the upper abdominal zone. Systolic epigastric throbbing may be 
due simply to overaction of the heart, or to congenital shortness of 
the sternum, owing to which the anterior surface of the right ventricle 
beats against the soft structures' of the epigastrium, rather than 
against bone. The same sign may indicate right ventricular hyper- 
trophy and dilatation, or a displacement of the heart to the right by 
one of the causes enumerated above. Postsystolic pulsations originate 
in the abdominal aorta, commonly as the result of the so-called 
dynamic pulsation of this vessel, such as is encountered in neurasthenia 
and in severe anemia. Aneurism of the abdominal aorta, enlarged 
peritoneal lymphatics, tumors of the liver, stomach, gut, and pan- 
creas, as well as tightly impacted fecal masses overlying the aorta., 
all may transmit the throb of this artery as an epigastric pulsation 
occurring a trifle later than the ventricular systole. 

Pulsation of the liver is practically a pathognomonic sign of tri- 
cuspid regurgitation, though its occurrence in connection with this 
lesion is by no means constant. The throb of a pulsating liver is 
felt in the right h)^pochondrium (not merely in the epigastrium), 
below the lower costal border, and is most readily detected 
by bimanual palpation. The time of such a pulsation is tardily 
systolic, and its character is expansile — not merely a lifting thrust, 
like that of a liver jogged by a forcible heart-beat; it reflects the 
heart's impulse communicated, by fault of a leaky tricuspid orifice, 
through the inferior vena cava to the hepatic veins, with a conse- 
quent rhythmic distention of the liver directly after systole. 

Abnormal Areas of Retraction. — Broadbenfs sign, or a systolic 
retraction of the tenth and eleventh intercostal spaces below the 
left scapula, sometimes attended by a synchronous tug upon the 
eleventh and twelfth ribs, was first described by the younger 
Broadbent as an indication of chronic adhesive pericarditis, in 
which condition the diaphragm, anchored by dense adhesions to 
the pericardium, is dragged upward with each systole of the hyper- 
trophied heart, so that the diaphragmatic attachments to the chest- 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 333 

wall are pulled inward and retracted (Fig. 126). This sign must 
be carefully distinguished from a similar systolic retraction due to 
the tug of an hypcrtrophied or a greatly overacting heart, and met 
with especially in emaciated subjects, as Tallant has shown. 
Broadbent's sign is commonly attended by systolic retraction of 
the seventh and eighth ribs and intervening interspace near the 
left parasternal line, by systolic dimpling in the region of the apex, 
and by respiratory immobility of the epigastrium. 

In aortic regurgitation a systolic retraction over the precordia, due 
to atmospheric pressure, is sometimes demonstrable; and in some 
cases of mitral stenosis a late diastolic retraction is visible in the 




26. — Local systolic retractions of the thorax due to adherent pericardium. 



same situation. Recessions of this sort, which are due simply to 
sudden depression of the parietes provoked by strong pulsation, are 
to be discriminated from the cardiac tug exerted upon the chest- 
wall by an adherent pericardium. 

Venous Engorgement. — Circumscribed venous engorgements arise 
in consequence of local interference with the venous current, the 
stasis thus established being shown by the distended, tortuous con- 
dition of the superficial veins draining the area peripheral to the 
point of obstruction. The undue prominence of the surface veins 
and their tendency to form anastomoses upon the anterior thoracic 
wall in cases of mediastinal tumor (Fig. 50), and the abnormal size 



334 PHYSICAL DIAGNOSIS 

of a venous trunk distal to a thrombotic obstruction, are exam- 
ples of the changes wrought by local obstructions to the venous 
circulation. 

Engorgement of the jugular veins occurs as a physiologic respiratory 
phenomenon and as the result of pathologic interference with the 
venous return flow into the right auricle. The normal inspiratory 
acceleration and expiratory delay in the venous current can be 
demonstrated by inspection of the external jugular veins while the 
subject breathes forcibly and deeply, from the effects of which the 
jugulars become appreciably fuller during expiration, or the period 
of normal venous retardation. The vascular stress incident to chronic 
cough and dyspnea exaggerates this respiratory phenomenon and ulti- 
mately creates permanent distention of the jugulars, as in asthma, 




Fig. 127. — Jugular engorgement (Jefferson Hospital). 

emphysema, and other chronic affections of the bronchopulmonary 
structures. Inspiratory overfulness of these veins — the reverse of their 
normal state — may accompany mediastinopericarditis and medias- 
tinal tumor, indicating compression or traction of the intrathoracic 
venous trunks (KussmauPs sign). Habitual jugular enlargement 
from lesions that obstruct the flow through the veins into the heart, 
suggests, if bilateral, cardiac dilatation or compression of the superior 
cava, the innominate or the jugular veins by aneurism or by medi- 
astinal tumor; if unilateral, the sign points to compression of one in- 
nominate or jugular vein, as by a neoplasm or by an enlarged gland. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 335 

Enlargement and tortuosity of other superficial veins — notably, 
those of the upper thorax and the arms, the costal arch, and the 
upper part of the abdomen — have been specially dealt with else- 
where. (See pp. 107, 108.) 

General venous engorgement, ultimately attended by edema of the 
congested parts, points to cardiac enfeeblement the precise character 
and degree of which are to be determined by examining the heart, 
especially the right side. 

Thrills. — A thrill is the tactile equivalent of a murmur, and, like 
the latter, has a point of maximum intensity and a definite incidence 
in relation to the cardiac cycle. Thrills are excited by blood-eddies 
churned into vibrations by the same lesions that account for the 
production of murmurs, and are distinguished by the palpating hand 
as a fine or rough vibration, somewhat like the purr of a cat — hence 
the terms, " f remissement cataire" and "Katzenschtirren." In 
studying a thrill the palm of the hand or the finger-tips should be 
applied, with moderate pressure, to the surface of the chest, and the 
patient instructed not to breathe while the examiner times the occur- 
rence of the sign, and notes its situation, extent, quality, and point 
of greatest intensity. 

Thrills at the base of the heart may be symptomatic of aortic and 
pulmonary valvular defects, of aortic roughening, dilatation, and 
aneurism, and of Graves' disease. At the second right intercostal 
space, close to the sternal border, a systolic thrill, often carried upward 
into the carotids, is found in aortic stenosis and in roughened aorta; 
while if diastolic, and conducted down the sternum, a thrill in this 
site may denote aortic regurgitation. A systolic thrill in the second 
left interspace at the sternal edge occurs occasionally in pulmonary 
stenosis, and commonly in exophthalmic goiter; and a diastolic 
thrill in the same area may mean pulmonary regurgitation. Aneu- 
rismal thrills may be felt over the entire upper and middle precordia, 
and usually also in the arteries of the neck and in the episternal 
notch; in the latter depression the systolic thrill of a dilated aorta 
may also be perceptible. 

Thrills at or near the apex of the heart are due generally to lesions 
of the mitral valves; less commonly they are transmitted from the 
base of the heart. If systolic, an apical thrill commonly indicates 
mitral regurgitation, or, very rarely, aortic stenosis; if presystolic, 
it is an almost certain sign of mitral stenosis, much less commonly 
being due to a Flint murmur of Corrigan's disease (q. v.) or to a 
functional disorder (see p. 461) ; if diastolic, it may represent the 
conducted thrill of aortic leakage. 



336 PHYSICAL DIAGNOSIS 

Thrills over the xiphoid and lower sternal region, systolic in time, 
can be demonstrated in many cases of organic tricuspid regurgita- 
tion and of dilatation of the tricuspid orifice. Tricuspid stenosis 
sometimes accounts for a presystolic thrill in this situation. 

Friction Fremitus. — Fremitus due to the rubbing together of 
roughened pericardial or pleural surfaces is perceptible as a deli- 
cate crackling or coarser creaking sensation, of a much more cir- 
cumscribed and superficial character than that of a thrill. 

Pericardial friction fremitus generally is distinguished by a to-and- 
fro rhythm, which, however, bears no definite relation to the heart- 
sounds; it is most distinctly felt, as a rule, between the second and 
fourth intercostal spaces, at and near the left sternal border; and it 
is exaggerated by pressure with the palpating finger and by making 
the patient bend forward. (See Fig. 159.) 

Pleuropericardial friction gives rise to fremitus synchronous with 
the heart-sounds, being especially well related to tjtie ventricular 
contractions; it is generally most distinct over the area corresponding 
to the tongue of lung overlapping the heart between the fourth and 
sixth ribs. According to the pleural reflection implicated, whether 
pulmonary or costal, pleuropericardial friction is palpable during 
either inspiration or expiration. (See Figs. 91 and 92.) 

Tracheal Tugging. — Compresson of the left bronchus by an 
aortic aneurism, and adhesions between an aneurismal sac and the 
trachea or bronchi, cause a slight descent of the windpipe with 
each pulsation of the aorta. This downward movement of the 
trachea is in turn transmitted to the larynx, the systolic depression 
of which is appreciated on palpation as a distinct tug synchronous 
with cardiac systole. Sometimes this indication of tracheal tugging 
(Oliver's sign) is visible, as well as palpable, and, exceptionally, it 
has a diastolic rhythm. The sign is elicited by supporting and 
elevating the cricoid cartilage with the thumb and forefinger, the 
patient meanwhile closing the mouth and raising the chin, so as to 
stretch the trachea and keep it tense. The tug can also be appre- 
ciated by grasping and elevating the body of the hyoid bone (M. 
L. Graves). 

Tracheal tugging, though most suggestive of aneurism of the 
thoracic aorta, cannot be regarded as pathognomonic, inasmuch as 
it has been met with in simple dilatation of the aortic arch and in 
pulsating mediastinal sarcoma. Actual downward traction of the 
trachea is to be distinguished from a spurious tug due, for instance, 
to carotid, thyroid, or innominate pulsation. 

The Arterial Pulse. — The pulse-beat corresponds to the wave 
of increased intra-arterial pressure excited by ventricular systole, 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM S37 

the tactile impressions thereby afforded being due to alteration in 
the shape and increase in the diameter of the artery's lumen. Of 
these changes the first, which alters the vessel's lumen from a flat 
to a circular shape, is the predominant factor of the pulse-beat, 
for the expansion of the artery is too insignificant to be appreciated 
by palpating a peripheral vessel, such as the radial artery. 

The normal pulse beats at the rate of about 70 to 75 a minute in 
the adult male, being somewhat more frequent in women and much 
more so in children. The pulsations, which follow a rhythmic 
sequence, occur synchronously at both wrists, and are of well-sus- 
tained volume and moderate force. Save when the vessel is unusually 
large and superficial, its structure cannot be felt. A clinical analysis 
of the pulse requires minute attention to the following details: the 
condition of the arterial wall and the size of the vessel; the pulse-rate, 
rhythm, tension, and volume; and the bilateral symmetry of the 
pulses and their relation to cardiac systole. 

Technic of Feeling the Pulse. — With the patient's forearm turned 
in partial supination and supported at the level of the heart, the 
first three fingers of the examiner's hand are pressed lightly against 
the radial artery at the wrist. The points to be investigated should 
be studied individually and with proper deliberation, for the feeling of 
the pulse is not merely a mechanical act, but one demanding both 
skill and experience linked with a keen appreciation of cardiovascular 
functions, normal and disordered, and the ability to correlate them 
with the tactile impressions perceived at the wrist. The condition 
of the arterial wall and the size of the artery are readily discovered 
by simple palpation and by " fingering" the vessel — which means 
gently sliding the pad of the finger across it transversely and along 
its course longitudinally, varying the pressure meanwhile so as to 
roll the artery against the bone. By these maneuvers, changes 
such as diminished elasticity, tortuosity, and mural irregularities, 
are made perfectly plain. The pulse-rate is ordinarily estimated 
by counting the number of beats felt during twenty seconds and 
multiplying them by three, but when the pulse is notably arhythmic, 
slow, or fast, it is a better plan to count it for a full minute. Some 
clinicians calculate the rate of an excessively rapid pulse by indicating 
each beat by a lead-pencil dot, and subsequently counting the number 
of dots made during a stated period. A general idea of the rhythm 
of the pulse is gained at the time its rate is counted, and should 
irregularity be found, the type should be carefully identified by a 
further digital examination, supplemented, in suitable instances, 
by sphygmography. The arterial tension may be approximated 



338 PHYSICAL DIAGNOSIS 

by noting the pressure required to obliterate the pulse-beat, the 
manner of obtaining this information consisting in gradually increas- 
ing the pressure of the proximal finger until the middle finger fails 
to feel pulsation, the distal finger meanwhile exerting firm pressure 
below, in order to block peripheral waves. The sphygmomanometer 
must, of course, be employed for accurate measurements of the 
blood-pressure. (See p. 31.) The volume of the pulse is judged 
by palpating with gentle pressure, at first uniform and then progres- 
sively increased, with a view to ascertaining the amount of dis- 
tention that the artery undergoes with each systole of the ventricles. 
The synchronism and comparative force of the two radials are shown 
by bilateral palpation, while the relation of the pulses to cardiac 
systole is learned by simultaneous radial and precordial palpation. 




Ventricular systole Aortic valve closure 

Fig. 128. — Sphygmogram of the normal radial pulse: a-b, Upstroke; b-e, down- 
stroke; b, apex; c, predicrotic (tidal) wave; d, dicrotic (recoil) wave. (Tracing by 
Dr. G. Bachmann.) 

Clinical Significance of the Sphygmogram. — The following 
details of the radial sphygmogram serve as a basis for the interpreta- 
tion of various changes produced by diseases of the cardiovascular 
system (Fig. 128; cf. Fig. 14). The special tracings, some of 
which have quite a distinctive relation to certain types of valvular 
disease and cardiac arhythmia, are discussed in connection with 
these conditions in Section VI. 

The Course of the Base Line. — The substitution of a wavy base 
line for one which runs a straight course is met with in conditions 
of dyspnea and subnormal blood-pressure, the undulations rising 
with expiration and falling with inspiration. 

The Angle of the Apex. — A sharp apex with an unusually acute 
angle designates low arterial tension and a free peripheral blood- 
flow, while a blunt or rounded apex having an obtuse angle is a sign 
of high tension and obstruction to the peripheral circulation. The 
former accompanies the vigorous systoles and relaxed arterial ten- 
sion of Corrigan's disease, and the latter is commonly due to arterio- 
sclerosis, aortic stenosis, and aneurism. It is important also to 
remember that a blunt apex tracing is frequently the result of ex- 
cessive tension of the sphygmograph spring or of a misfit between 
the metal pad of the instrument and the patient's artery. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 339 

The Spacing, Height, and Direction of the Upstroke. — RegulaF 
spacing of the upstrokes means rhythmic beating of the pulse, the 
rate of which may be determined either by counting the strokes of 
the stilet or by attaching a chronograph to the sphygmcgraph. 
Arhythmia is shown by irregularity in the length of the upstroke 
intervals, which should be carefully measured with a pair of dividers 
in order to fix the degree and the type of the arhythmia in the case 
in question. A spurious form of arhythmia may be produced by 
some fault in the mechanism that drives the smoked paper slip, 
which if it travels too fast, imitates the closely spaced strokes of a 
rapid pulse, or which, if it moves too slowly, simulates the wide 
spacing of a slow beat. 

The height of the upstroke is a rough index of the pulse volume, 
the stroke being either long or short according to whether the volume 
be ample or deficient. A perpendicular upstroke, the apex of which 
is very high above the base line, reflects vigorous contraction of the 
left ventricle. Decided obliquity of the upstroke suggests some 
impediment to the normally vigorous impact of the systolic blood- 
column, the slow distention of the arteries being referable to such 
factors as weakness of the left ventricle, high arterial tension, aortic 
stenosis, mitral insufficiency, or aneurism. In studying the upstroke 
it must always be remembered that this detail of the sphygmogram 
varies with the tension of the wrist-band and the spring of the instru- 
ment, as well as with the approximation, exact or imperfect, of the 
metal plate to the patient's artery. 

The Strength of the Downstroke Waves. — A diminutive tidal wave 
indicates diminished force or volume of the arterial blood-flow, as, 
for example, in simple cardiac asthenia, in undue peripheral relaxa- 
tion, and in regurgitant defects of the aortic and mitral valves. An 
exaggerated tidal wave, on the other hand, suggests high arterial 
tension, as in conditions attended by fibrosis and atheroma of the 
arteries. A feeble recoil wave occurs in high arterial tension, and 
the level of such a wave is abnormally high above the base line ; 
in states of low tension this wave is comparatively well marked. 
Numerous oscillations and subsidiary downstroke waves are fre- 
quently observed on the tracing as a consequence of a high-tension 
pulse. 

Changes in the Arterial Wall and Caliber. — The diminished 
resiliency of a sclerotic arterial wall conveys to the palpating finger 
a sense of increased resistance which becomes more and more striking 
as the fibrosis progresses, until finally the affected vessel is converted 
into a rigid, tortuous tube, either more or less symmetrically thickened 
or beaded with spots of local calcification. A sclerotic and a high- 



34o 



PHYSICAL DIAGNOSIS 



tension vessel are distinguishable by suppressing the pulse-beat 
with the proximal and distal fingers, while the mural condition is 
examined with the middle finger. Since peripheral sclerosis does 
not necessarily imply similar implication of the deeper arteries, such, 
as the aorta and the coronaries, thickening of the radials alone does 




Fig. 129. — Brachial arteriosclerosis. (Jefferson Hospital.) 

not warrant a diagnosis of general arteriosclerosis, to detect which 
all the accessible arteries, as well as the heart, should be examined. 

Changes in the size of the vessel, due to increase in its caliber, are 
closely related to the volume of the pulse, to be referred to later, 
although personal peculiarities also account for variations in the 
size of the arteries, quite apart from cardiovascular influences. 

Disturbances of the Pulse-rate. — Fundamentally, deviations 
from the normal pulse-rate are referable to defective function of the 
controlling nerves of the heart and to variations in arterial tension. 
Thus, the pulse beats with increased frequency if the sympathetic 
nerves of the cardiac ganglia are excited by stimulation, if the 
vagus loses its restraining influence through depression, or if the 
vis afronte is lessened by subnormal arterial tension. On the con- 
trary, the pulse-rate is slowed by depression of the sympathetic or 
of the ganglia, by stimulation of the vagus, and, usually, by the 
increased effort of the heart provoked by high arterial tension. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 34 1 

Increase of the pulse-rate, giving rise to the pulsus frequens, is 
symptomatic of the abnormally rapid cardiac action known as 
tachycardia (Fig. 130, 1). Exceptionally there are persons who can 
voluntarily accelerate the pulse-rate, perhaps by a psychic in- 
fluence upon the vagus and the accelerator nerves. Increased fre- 
quency of the pulse attends, with a certain parallelism, most 
febrile states, the pulse rising about eight beats above normal for 
each degree of fever, and in children attaining even a higher ratio. 
To this general rule there are numerous exceptions, notably yellow 
fever, tuberculous meningitis, pneumonia, and enteric fever, in all 
of which hyperpyrexia and a relatively slow pulse may coexist. The 
same is often true of fevers complicated by uncompensated car- 
diovascular diseases. On the other hand, the pulse-rate is frequently 
found to be disproportionately high to the pyrexia in sepsis, phthisis, 
scarlatina, and acute miliary tuberculosis. Nervous disturbances 
commonly account for a rapid pulse, as in the neurasthenias, so-called 
irritable heart, nervous palpitation, paroxysmal tachycardia, and 
Graves' disease. Undue frequency of the pulse is also a familiar 
sign in locomotor ataxia, anterior poliomyelitis, acute ascending 
paralysis, cerebral concussion, vagus neuritis and compression, and 
sympathetic irritation. Pain, whatever its cause, generally accounts 
for tachycardia of more or less degree. Circulatory defects, due to 
valvular or mural lesions of the heart, to pericarditis, to cardiac 
displacement, and to the state of collapse, greatly disturb the pulse- 
rate, variously exciting increase or a diminution, as well as interfering 
with the normal rhythm. One looks for a quick pulse after hemor- 
rhage, after aspiration of a large exudate, in the essential anemias, 
in Addison's disease, and in arthritis deformans. Other factors 
of abnormal pulse rapidity include the toxic effects of belladonna 
and aconite, and, in most persons, the immoderate use of alcohol, 
tea, coffee, and tobacco acts similarly, though in others just the 
opposite effect may be produced. 

The atropin reaction, or an increase in the pulse-rate by the ac- 
tion of atropin on the vagus, is sometimes used by clinicians as a 
test of cardiac competency. If the integrity of the heart be un- 
impaired, the pulse-rate increases from 30 to 40 beats per minute 
within one-half hour after a hypodermic injection of from -5V to -fa 
grain of atropin, but in a subject of myocardial degeneration no such 
acceleration occurs. This test is used by Talley in cases of auricular 
fibrillation (v. i) to determine whether vagal tone or cardiac muscle 
is the main factor, and he finds in such cases after full digitalization 
that atropin, after a preliminary period of slowing of the pulse, 
subsequently accelerates it if the vagus be at fault, while a much 



342 



PHYSICAL DIAGNOSIS 



less marked reaction is noted if the cardiac muscle be structurally 
diseased. A similar release of the vagal action has been observed 
in the slow pulse of meningitis (Roch and Cottin). Amyl nitrite, 
which has the advantage of instantaneous effect, has an action 
similar to that of atropin, and can be used as its substitute under 
identical conditions. 

In judging a pulse-rate the accelerating influence of mental 
unrest, physical exertion, and the digestive period should be taken 
into account. It is not without interest also to remember that a 
normal pulse perceptibly quickens as the result of violent coughing, 
as well as after Valsava's experiment of forced expiration with the 
mouth and nose closed. 

Auricular tachycardia is met with in auricular flutter, a condi- 
tion in which the normal auricular contractions are replaced by 




Fig. 129a. — Electrocardiogram of auricular flutter. (Tracing by Dr. E. B. Krumbhaar.) 

abnormal impulses, of rapid rate and perfect rhythm, springing 
from auricular foci away from the sino-auricular node, and occur- 
ring at a rate of from 200 to 300 or more beats per minute. So 
accelerated are these new systoles of the auricles that true dias- 
tole of these chambers cannot take place, and ordinarily but a 
part of the contractions are shared by the ventricles, for many of 
the waves are blocked by the bundle of His. While the auricles 
beat at a 300-per-minute rate, the ventricles may beat but one-half 
or one-fourth as fast, though exceptionally a temporary (and 
dangerous) phase develops wherein the ventricular pulse equals 
the auricular rate. Chronic myocarditis, arteriosclerosis, and a 
history of rheumatism, syphilis, or gout are the common ante- 
cedents of this type of tachycardia, which is commoner in the aged 
than in the young. It is prone to persist for years, and, as Lewis 
points out, "a constant repetition of the same high pulse at inter- 
vals of weeks or months" strongly suggests the presence of such 
a lesion. In some cases the rapid auricular beats are clearly be- 
trayed by jugular pulsations in the neck, and deep pressure in the 
carotid region, so as to irritate the vagus, causes an appreciable 
slowing and intermission of the arterial pulse. A full dose of digi- 
talis acts similarly. 

On the sphygmogram numerous a-waves of regular contour and 
height fill the diastolic (Vf) period of the tracing, and the .arte- 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 343 

rial waves vary in regularity and number, depending upon the 
integrity of the heart's conduction path. The electrocardiogram 
shows a multiplicity of small, sharp P- waves of undue rapidity 



Fig. 1296. — Electrocardiogram showing leads I, II, III of auricular flutter with in- 
complete heart-block and extreme tachycardia. Note uniformity, definition, and 
incidence of P-waves, and irregularity and variable height of i?-waves. Auricular rate 
600, and ventricular rate 200, per minute. (Tracing by Dr. E. B. Krumbhaar.) 

and striking regularity ; or the oscillations immediately preceding 
the ventricular complex may be so rapid and delicate as to form 
merely a blurred streak before the i^-waves (Fig. 1 29a) . The latter 
are grouped irregularly, or are typical of an orderly incidence 
between every third or fourth auricular undulation, according to 
the degree of existing heart-block. The accompanying electro- 
cardiogram (Fig. 1296) illustrates the irregularity of the waves in 
leads I, II, III in a case of auricular flutter with delayed and 
intermittent conduction of the impulses. 

Paroxysmal tachycardia is a condition which arises in response 
to new and abnormal impulses originating in foci far removed from 



344 PHYSICAL DIAGNOSIS 

the sino-auricular node, whose action is overshadowed by that of 
the ectopic stimuli which excite a pulse-rate varying from ioo to 
200 beats per minute, in paroxysms lasting from a few seconds to as 
long as many hours or even days. As a rule, this rapid rate is 
initiated in the auricle, less commonly in the ventricle, but in 
either event it remains rhythmic, despite variations in the force 
of the individual arterial [pulse-beats. The paroxysms of tachy- 
cardia begin most abruptly and end with equal suddenness, and but 
immaterial acceleration of the pulse is provoked by physical exer- 
cise. Mental and physical stress, flatulence, and gastro-intestinal 
disorders usher in most attacks, and myocardial degeneration, 
coronary artery sclerosis, and mitral stenosis are familiar findings 
in those cases in which pathologic defects are found. 

The arterial sphygmogram clearly indicates the onset of the 
paroxysm by a line of exceedingly rapid and small waves of equal 
height, often preceded by a few premature auricular systoles. 
The venous tracing shows corresponding rapidity, and may be 
either undisturbed or demonstrate obliteration of the ^-waves by 
the a-waves. In the electrocardiogram there are numerous ven- 
tricular complexes which tend to encroach upon and even to oblit- 
erate the preceding P-waves, whose increased height and inversion 
are sometimes conspicuous. 

Diminution of the pulse-rate, betrayed by the pulsus rarus, signi- 
fies an unduly slow cardiac action termed bradycardia (Fig. 130, II). 
In certain individuals this condition does not appear to be un- 
natural (Napoleon's pulse averaged but 40 beats per minute), and 
a pulse-rate of 50 or 60 a minute may exist habitually without 
being of itself incompatible with perfect health; any noteworthy 
diminution below these figures, particularly if it persists, calls for 
inquiry as to some pathologic factor. In studying the slow pulse it 
is essential to determine that the peripheral pulsations are a true 
index of the contractions of the heart: impairment of the cardiac 
power may be of such a character that only the alternate ventric- 
ular systoles are strong enough to produce a perceptible radial 
pulse, thus creating a fictitious pulsus rarus. An inordinately slow 
pulse is symptomatic of various disorders of the heart and blood- 
vessels, and of these factors it is well to remember fibroid and fatty 
heart, coronary artery sclerosis, general arterial sclerosis, aortic 
stenosis, and Stokes-Adams disease. Many nervous diseases are 
commonly attended by the pulsus rarus — meningitis, cerebral tumor 
and hemorrhage, depressed fracture of the skull, lesions of the 
medulla and of the upper cord, epilepsy, mania, paresis, and myx- 
edema. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 345 

Extreme bradycardia with syncope is a cardinal physical sign 
of poisoning with the newer asphyxiating cyanogen gases of modern 
warfare, and similar effects are caused by the products of incomplete 
hydrocarbon combustion, in intoxication by motor gases. 

A slow pulse is generally found during the apneic period of 
Cheyne-Stokes respiration, in the postfebrile stages of many 
acute infections, in grave cachexias, in the toxemias of icterus, 
diabetes, uremia, ergotism and saturnism, and in poisoning by 
digitalis, strophanthus, convallaria, conium, and opium. Pain, 
which generally accelerates the pulse, and chronic indigestion, 
which acts similarly, may under certain circumstances consider- 
ably retard its frequency. 

The combination of bradycardia, diminished pulse volume, and 
hypotension constitutes the oculocardiac reflex of Aschner, a 
phenomenon attributable to a true trigeminovagus reflex action. 
This trilogy of signs, notably the slowing of the pulse 8 to 10 beats 
a minute, occurs promptly in fully 70 per cent, of healthy subjects 
after firm compression of the eyeball with the pulp of the finger. 
The reaction is within normal limits in nervous bradycardia, in 
states of arterial hypertension, and in most cases of paroxysmal 
tachycardia, although Lian finds that it is sometimes possible to 
slow the heart in the last-named disorder by prolonged bilateral 
ocular pressure. The oculocardiac reflex is lost, as a rule, in tabes ; 
and it is conspicuous in Graves' disease, in epilepsy, in gastro- 
intestinal neuroses, and in various toxemias, notably in nico tin- 
poisoning. An "inverted" reflex, distinguished by an acceleration 
of the pulse after ocular compression, has been observed in incipi- 
ent cases of exophthalmic goiter and in many emotional states. 

Irregularity and Intermission. — The radial pulsations, which 
normally take place at regular intervals coincident with ventric- 
ular systole, are subject to various disturbances of rhythm con- 
sisting of irregularities and intermissions, conforming in certain 
instances to well-defined types. On the other hand, there are also 
pulse irregularities that lack definite sequence in their series of 
beats, and in which the tempo is much disordered, the individual 
beats being separated by a confusion of long and short intervals. 
Pulse irregularity indicates some impairment, either functional or 
structural, of the cardiac force, whereby its contractions deviate 
from their normal periodicity and generally also fail in power, 
the irregularities of time being attended by inequalities in the 
volume and power of the separate beats. As already intimated 
in a preceding paragraph, an intermittent pulse is not an infallible 
sign of an intermittent heart, since the systoles, though rhythmic, 



346 PHYSICAL DIAGNOSIS 

may not all produce an appreciable pulse at the wrist. The 
pulsus intermittens, a general term for intermissions of the periph- 
eral pulse, must always be distinguished, by auscultation of the 
heart, from the pulsus deficients, in which the intermission depends 
upon actual failure of the heart to contract. An allorrhythmic 
pulse is distinguished by rhythmic irregularities, or those in which 
the disordered pulse rhythm is definitely systematic and periodic 
{pulsus inequalis periodicus) . To this type belong the bigeminal 
pulse {pulsus bigeminus), distinguished by two beats and a pause, 
and the trigeminal pulse {pidsus trigeminus) , consisting of three beats 
and a pause, recurring in orderly succession, these peculiar allorrhyth- 
mias being most commonly found in mitral disease, especially after full 
doses of digitalis or one of its cogeners (Fig. 130, iv, v). The inter- 
ruption of a rhythmic sequence of beats by a minor beat distinguishes 
the pulsus intercidens. In the alternating pulse {pulsus alternans) there 
is a series of strong and feeble beats alternating in regular succession. 
This type of pulse, which Lewis prefers to designate alternation of 
the heart, is most often found in the aged, and is a grave sign, 
in that it indicates a progressive exhaustion of the cardiac muscle, 
attending lesions such as arteriosclerosis, myocardial fibrosis, 
angina pectoris, and chronic nephritis. The use of the sphyg- 
momanometer in clearly identifying the alternating pulse has been 
referred to elsewhere. (See p. 34.) 

The paradoxic pulse of Kussmaul {pulsus paradoxus) , character- 
ized by bilateral enfeeblement or disappearance of the radial pulse 
during inspiration, is not distinctive of any special condition, though 
it is not uncommonly demonstrable in adhesive pericarditis, pericar- 
dial effusion, mediastinal inflammation and tumor, and extreme 
cardiac asthenia. Sometimes Kussmaul's pulse may be closely 
imitated at will simply by holding the breath after having taken a 
deep inspiration. Inspiratory disappearance of one radial pulse has 
been noted in adhesion of the subclavian artery to the pleura. 

In seeking for a cause of an irregular pulse, it should be remem- 
bered that this peculiarity may be of no consequence whatever, 
especially when it appears temporarily. It is frequently traceable to 
emotional disturbances, physical strain, neurasthenia, indigestion, 
constipation, and the misuse of tobacco, tea, and coffee. Old people 
and young children sometimes have a persistently irregular pulse, 
with nothing tangible to account for it. But it is another story 
when, aside from these influences, the subject's arhythmia is con- 
stant and associated with subjective symptoms and with signs of 
cardiac disturbance, under which circumstances one naturally in- 
vestigates first the cardiovascular and then the nervous systems. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 347 

These sources of an irregular pulse are referred to under Cardiac 
Arhythmia. (See p. 371.) 

Variations in the Tension, Volume, and Velocity of the Pulse. 

— Tension. — The tension of the pulse-wave is regulated by the force 
and rate of the ventricular systole and the volume of blood thereby 
propelled, by the degree of peripheral resistance, and by the elasticity 
of the arteries. Thus, a powerful, rapid heart and a well-contracted 
set of peripheral vessels together make for inordinately high tension — 
hypertension ; while a feeble, slow heart and a toneless, relaxed 
vasomotor system give subnormal tension — hypotension. In most 
instances these factors are not so well balanced as in the academic 
illustrations just drawn, for, owing to their unequal action, the 
effects of certain factors tend to be neutralized by the influences of 
others — normal arterial tension may be preserved even in collapse, 
should the hypotension of the vasomotor depression be negatived 
by the recuperative overaction of the heart. Usage establishes 
the terms pulsus durus and pulsus mollis, the former designating the 



Fig. 129c. — Electrocardiogram of a case of arterial hypertension, showing the large 
T-wave of vigorous ventricular contraction. (Tracing by Dr. T. A. Cope.) 

tense, hard, non-compressible pulse of hypertension, and the latter 
denoting the relaxed, soft, readily compressible pulse of hypotension 
(Fig. 130, VI, VII). Of the latter, two special types have been 
described: the extraordinarily soft and empty gaseous pulse, and 
MounereVs pulse, soft, slow, full, and quite distinctive of the toxemia 
of icterus. 

Clinically, it is desirable to estimate the maximum or systolic, 
the minimum or diastolic, and their difference or the pulse, pressures, 
data accurately obtainable only by using a sphygmomanometer. (See 
p. 31.) Only roughly is it possible to gage arterial tension by 
ordinary digital examination, though some general idea, later to be 
elaborated instrumentally, may be gained by compressing the radial 



I. Pulsus frequens. 



II. Pulsus rarus. 




III. Pulsus inequalis. 




V. Pulsus trigeminus. 



VI. Pulsus durus. 




348 



VIII. Pulsus dicroticus. 




IX. Pulsus anacroticus. 




X. Pulsus bisferiens. 




XI. Pulsus magnus. 



XII. Pulsus parvus. 



XIII. Pulsus celer. 



XIV. Pulsus tardus. 

Fig. 130. — Sphygmograms of pathologic types of the arterial pulse. (Tracings by 
Dr. G. Bachmann.) 

349 



350 PHYSICAL DIAGNOSIS 

artery in the manner described above, and by noting both the force 
of the pulse and the fulness of the vessel between the beats. Thus, 
with three fingers laid upon this vessel, the degree of pressure exerted 
by the proximal finger to obliterate the pulse approximates the 
systolic pressure, provided that the pulse under examination is not 
of too full a volume. Using the same technic, the diastolic pressure 
is suggested by estimating the force necessary to bring out the 
greatest impact of the pulse-beats, which, as the pressure of the 
fingers increases, gradually becomes stronger and stronger, attains 
an acme, and then diminishes. It is also worthy of note that a 
radial artery palpable between pulse-beats suggests hypertension, 
and that one which is indistinguishable indicates hypotension, the 
influence of fibrocalcareous changes being, of course, excluded. 

In a pulse of low tension and usually of full volume the dicrotic 
or recoil wave is frequently appreciable, by gentle palpation, as a 
secondary impact immediately following the principal beat. This 
exaggeration of the normal dicrotic wave {pulsus dicroticus) is well 
shown in febrile states and exhaustion attended by extreme arterio- 
capillary dilatation, in uncompensated mitral regurgitation which 
restricts the ventricular output of blood, and in posthemorrhagic 
anemia severe enough to diminish the volume of arterial blood 
(Fig. 130, VIII). The pulse is described as hyperdicrotic when the 
dicrotic wave of the sphygmogram falls below the base of the sys- 
tolic upstroke, and a pulse of this sort suggests very low tension and 
increased cardiac rate and force. 

Occasionally, as the result of hypertension and tardy filling of 
the aorta (as in extreme aortic stenosis) , the predicrotic or tidal wave 
is palpable just after the systolic beat {pulsus bisferiens). That 
this predicrotic impact is associated with high tension and is most 
distinctly developed by firm pressure upon the artery serves to dis- 
tinguish it from the dicrotic wave, which accompanies low tension 
and is detected only by gentle or moderate pressure. A tracing of 
the pulsus bisferiens shows a double apex composed of upstroke 
and tidal wave, the latter sometimes being the more conspicuous 
(Fig. 130, X)^ 

Another variety of high-tension pulse, also met with in aortic 
stenosis, is characterized by a notched upstroke or anacrotic limb, 
and hence is known as the pulsus anacroticus (Fig. 130, IX). The 
upstroke interruption of this type of pulse means, according to 
Mackenzie, " that the lever of the sphygmograph has been raised 
in the first instance slightly quicker than the following current of 
blood, and as the distending wave increases, the returning lever is 
caught and carried along to the summit." The anacrotic pulse, 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 35 1 

then, reflects augmented contractile power at the end of systole, and 
does not indicate a real interruption of the ventricular contraction. 

In general, hypertension accompanies diffuse arterial sclerosis, 
cardiac hypertrophy, angina pectoris, apoplexy, uremia, nephritis, 
and adequately compensated aortic regurgitation. Hypotension is 
to be expected as the effect of shock and collapse, extensive frank 
or concealed hemorrhage, acute febrile diseases, exhausting cachexias 
and anemia, primary myocarditis, cardiac dilatation, and valvular 
lesions, such as extreme aortic stenosis and mitral leakage, which 
diminish the ventricular output of blood with systole. 

Volume. — The volume of the pulse, or the extent of the arterial 
expansion produced by the pulse-wave, varies with the size of the 
vessel's caliber and with the volume and force of the systolic blood- 
column. The more yielding the walls of the artery under the influ- 
ence of the systolic blood-wave, the greater the volume of the pulse, 
of which the chief determining factors are, apart from the size and 
force of the systolic wave, the degree of intra-arterial pressure and 
the inherent tension of the arterial walls. In general terms, then, 
it follows that with an equal systolic output of blood, peripheral 
dilatation and hypotension increase, and that peripheral constriction 
and hypertension diminish, the volume, or size, or amplitude of the 
pulse. In health, aside from the physiologic exaggeration during 
inspiration, the individual pulse-beats are of equal volume {pulsus 
equalis), and, unless modified by anatomic peculiarities, there is 
also a similar bilateral symmetry. Inequalities of volume (pulsus 
inequalis) are generally associated with irregularities of rhythm and 
rate, the causes of which have been dealt with sufficiently in a fore- 
going paragraph (Fig. 130, III). 

Increase of the pulse volume {pulsus magnus) commonly attends 
conditions provocative of subnormal arterial tension, and is recog- 
nized by the palpating finger as an unnatural expansion of the 
vessel at the time of the pulse-beat (Fig. 130, XI). Jerkily arhyth- 
mic pulsations of undue volume are sometimes spoken of as the 
"caprizant" or " goat-leap" pulse. The full, bounding pulse of 
fevers, the large pulse of cardiac overaction or hypertrophy, and the 
momentarily voluminous pulse of aortic valve leakage typify the 
pulsus magnus. Overfulness of the artery during the interval 
between pulsations {pulsus plenus) indicates a large volume of blood 
within the vessel, irrespective of its size — a small, tense, contracted 
artery may be just as full, relatively, as one which is large, soft, and 
relaxed. 

Diminution of the pulse volume (pulsus parvus) is attended by but 
slight stretching of the vessel-wall during the beat, and is not infre- 



352 PHYSICAL DIAGNOSIS 

quently combined with arhythmia and with increased arterial tension 
(Fig. 130, XII). A small pulse may depend upon deficient cardiac 
force, or upon lesions that diminish the volume of blood in the periph- 
eral vessels. The former accounts for the subnormal pulse volume in 
collapse, in conditions attended by malnutrition and exhaustion, and 
in the various functional and structural weaknesses of the heart; the 
latter explain the small pulse in stenoses of the aortic and mitral 
orifices, in aneurism, and in certain cases of profound anemia, the 
arterial blood-column being obstructed in the first instance, diverted 
in the second, and actually reduced in bulk in the last. The arach- 
noid pulse, small, thread-like, and running, is a good example of the 
excessive diminution of pulse volume symptomatic of extreme 
circulatory depression. A pulse whose volume and force gradually 
taper off has been described as the decurtate or mouse-tail pulse. 
Emptiness or collapse of the artery between beats is indicated by 
diminished amplitude of the pulse during such intervals {pulsus 
vacuus), and is dependent upon grave cardiac enfeeblement, or 
inadequate ventricular filling in mitral leakage, or an unsustained 
arterial blood-column due to aortic insufficiency. 

Velocity. — The rapidity with which the individual waves rise and 
fall is referred to as the velocity or celerity of the pulse. A quick 
pulse {pulsus celer), or one whose undulations are abrupt, gives 
rise to a series of sharp tapping beats, which, irrespective of their 
volume, quickly recede from the palpating finger. Subnormal arte- 
rial tension is suggested by this type of pulse, the steep, high strokes 
of which are clearly shown by the sphygmographic tracing (Fig. 
130, XIII). The trained observer has little difficulty in recognizing 
the pulsus celer without instrumental aid, if care be taken to differ- 
entiate the sharp bounding pulse of increased volume: the two may 
resemble each other in so far as the rise of the wave is concerned, but 
in the latter the pulse-wave, though sharp, lacks a rapid descent and 
is fairly well sustained. The pulsus celer may be symptomatic of 
arteriocapillary relaxation, incident, for example, to fever, collapse, 
debility, and anemia, but its acme is attained in the pulsus celerrimus 
of Corrigan's disease, in which left ventricular hypertrophy, relaxed 
peripheral vessels, and a leaky aortic orifice combine to create a 
poorly sustained pulse-wave of extraordinary velocity and volume. 
A tardy pulse (pulsus tardus) rises and falls slowly and is well sus- 
tained, independently of the frequency of its beats. The impact 
of this pulse, which is to be expected when the arterial tension is high, 
conveys to the palpating finger the sensation of a slowly rising wave 
of rather prolonged duration and deliberate fall, which peculiarities 
are traced by the sphygmograph as a curve of moderate amplitude, 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM $53 

oblique upstroke, rounded apex, and gently declining downstroke, 
marked by feeble secondary oscillations (Fig. 130, XIV). Pure 
aortic stenosis is the factor of the most typical examples of the 
pulsus tardus, owing to the slow ventricular contractions and de- 
layed passage of the blood-stream through the narrow aortic orifice. 
Arteriosclerosis, hindering the prompt rise and fall of the pulse- 
waves, is also an important cause of this type of pulse. 

Asymmetry of the Pulses. — Conditions that impede the normal 
passage of arterial blood-waves from the left ventricle to the periphery 
disturb the bilateral symmetry of the pulse-rate and volume, by 
retarding and diminishing the waves beyond, and on the same side as, 
the lesion, which in the extreme instance may produce so decided an 
obstruction to the blood-current as practically to extinguish the pulse 
in the distal arteries of the surface. Inequalities of the pulses from 
such causes must be carefully distinguished from those due merely 
to abnormal distribution of the vessel or vessels under examination; 
and it is also to be recalled that the left radial pulse is generally 
stronger in right-handed individuals and in the ambidextrous. 

Taking as criteria the radial arteries, delay and enfeeblement 
of one pulse at the wrist suggest aneurism, of the ascending aortic 
arch or of the innominate artery if the right pulse be modified, and of 
the transverse arch (to the left of the innominate's origin) or of the 
descending portion if the left pulse be altered. Aneurismal dilata- 
tion of the subclavian, axillary, or brachial arteries are also to be 
regarded as a possible, though rare, cause of suppressed peripheral 
pulsations on the same side, and a like asymmetry is referable to 
arterial obstruction by embolism or thrombosis, as well as to the 
pressure of cicatrices, faultily knit fractures, tumors, and intrathoracic 
effusion of fluid and of air. Retardation of both carotid pulses in 
comparison with the apex-beat is found in aneurism of the ascending 
aorta, while the right carotid beats later than the heart in aneurism 
of the innominate artery. Suppression of both femoral pulses may 
mean either aneurism of the abdominal aorta or, most exceptionally, 
congenital obliteration of this vessel; inequality in the force of the 
femorals suggests obstruction, as by thrombosis or tumor, of the feebly 
beating vessel; and delay of the femoral pulse, compared with the 
radial, suggests aortic aneurism below the arch. 

The Capillary Pulse. — The capillary pulse of Quincke, which 
indicates transmission of the individual pulse-waves to the capil- 
laries, is recognized as a systolic flushing and diastolic pallor of 
some peripheral part, such as beneath the finger-nail — hence the 
expression, pulsus subungualis. To show it in this situation the nail 
23 



354 PHYSICAL DIAGNOSIS 

should be blanched by slight pressure on its tip, whereupon systolic 
reddening of the pale subungual area is readily perceptible. The same 
thing can be seen upon the mucous membrane of the lower lip when 
it is everted and pressed upon with a glass slide, and along a line of 
hyperemia rubbed upon the forehead with some blunt instrument, 
such as the cap of a fountain-pen. If the ophthalmoscope be used, 
one can also observe a capillary pulsation of the retinal arteries. 

Ordinarily, no pulse is visible in the capillaries, through which the 
blood trickles in a waveless stream, but under circumstances that 
increase cardiac force, diminish capillary resistance, and retard venous 
return flow, the pulsations of the heart permeate as far as the small 
arteries of the periphery and distend them with each systole. Essen- 
tially, the capillary pulse is the product of the pulsus celer and is 
associated with conditions of subnormal arterial tension. It is a 
valuable sign of aortic regurgitation, though it is not constant in this 
lesion, nor pathognomonic, since a capillary pulse is demonstrable in 
many conditions underlying the pulsus celer, i. e., fever and anemia, 
and, moreover, it is occasionally noted in a presumably healthy person. 

The Venous Pulse. — Ordinarily, the auricular contractions driving 
the blood-stream into the ventricles fail to create any appreciable 
backward wave within the venae cavae and pulmonary veins, since 
at this period of the cardiac cycle the auricular outlets of these vessels 
are so tightly contracted that a reflux cannot take place. When, 
however, the veins are unduly distended and their cardiac orifices 
correspondingly dilated, the contractions of the heart propel blood- 
waves not alone forward into the arteries, but also backward into 
the great venous trunks, the superior caval impulses being propa- 
gated into the veins of the neck, especially on the right side, which 
show pulsatile movements, either presystolic or systolic in time, 
according to the mechanism at work, as will be explained presently. 
Occasionally the backward waves are blocked by the valves just 
distal to the jugular bulb, and in this event a "bulbous pulse" is 
observed at the root of the neck, above the sternoclavicular articula- 
tion. But usually these valves leak, so that there is visible pulsation 
of the jugular veins, more prone to occur in the internal jugular than 
in the external, though the latter's pulsations are more readily detected, 
owing to its superficial situation. The venous pulse thus produced 
serves as a definite index to the action of the right auricle and 
ventricle. 

The venous pulse should be studied while the patient is in recum- 
bency, with the object of ascertaining its precise site, extent, and 
time relation to the events of the cardiac cycle. Pulsation of the 
internal jugular vein may be very similar to that of the carotid artery, 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 355 

but the jugular pulse-wave rises gradually and falls very suddenly, 
frequently causing momentary recession of the overlying tissues at the 
site of the pulsation, while the carotid wave rises abruptly and forcibly 
but falls slowly and deliberately, and, moreover, is attended by 
unnatural arterial throbbing remote from the cervical region. A 
true venous pulsation travels upward from the root of the neck and 
produces distention and rhythmic throbbing of the vein, after it 
has been emptied from below upward by the finger, but if the pul- 
sation be transmitted from the carotid artery, pressure over the vein 
distends it and exaggerates the pulsation above the point of constric- 




Fig. 131. — Sphygmogram of the normal venous and arterial pulses. (Tracing by 
Dr. G. Bachmann.) 

tion below which the vessel collapses and becomes pulseless. These 
visual signs of the venous pulse, though suggestive, should be con- 
firmed by means of a graphic tracing, in order to fix the exact time 
of the movements with relation to those of the heart, and by instru- 
mental aid of this sort it is possible to determine these essential 
details, and to recognize two distinct types of the venous pulse, the 
auricular and the ventricular, which differ very materially, from a 
diagnostic and prognostic viewpoint. 

The auricular or presystolic venous pulse is due to the contraction 
of the right auricle, and represents a physiologic or negative type of 
pulsation, for it may occur in the healthy subject in consequence of 
temporary venous distention, induced, for example, by prolonged 
holding of the breath. The sphygmogram of this type of pulse 
(Fig. 132) is distinguished by a succession of inordinately high 
auricular waves (a), timed well in advance of the carotid impulse, 
as shown by the lower tracing, made simultaneously with that of the 
jugular movements. The systolic wave (s), following the closure of 



356 



PHYSICAL DIAGNOSIS 



the tricuspid valve (3-4) is of comparatively moderate amplitude, 
and, after the period of auricular filling (Af), is succeeded by a single- 
peaked ventricular wave (V), after which the ventricular filling (Vf) 
commences, completing the diastolic phase. Comparing this sphyg- 
mogram with that of the ordinary jugular pulsations (Fig. 131; 
cj. Fig. 14), it is apparent that the chief characteristics of the auricu- 
lar venous pulse are an exaggerated a-wave, a moderate s-wave, and 
a 7;-wave of pyramidal outline rather than doubly undulated. Clin- 
ically, this type of pulse means adequate nutrition, contractility, and 
force of the right auricle. 



T - 7 3 




L 


Jugular 

Carotid 1 Pf 
Time 77 50 Sec- 


af: .6 vi T ' N 

5 6(3 


3 

.6 1 . 

A- ■ 



Fig. 132. — Sphygmogram of the auricular or presystolic type of venous pulse. (Tracing 
by Dr. G. Bachmann.) 

The ventricular or systolic venous pulse is produced by the con- 
traction of the right ventricle, and typifies the variety of pulsation 
sometimes described as pathologic or positive. It may indicate 
tricuspid leakage, whereby with each ventricular contraction a 
reflux blood-column is propelled back into the right auricle and 
thence into the venous tributaries of this chamber; or it may be 
due not so much to actual tricuspid leakage as to instant filling of 
the auricle, because of excessive intravenous pressure. The appear- 
ance of such a pulse suggests auricular enfeeblement, with com- 
paratively well-sustained ventricular power, which, despite the 
coexistence of dilatation sufficient primarily to set up tricuspid 
regurgitation, is still strong enough to drive backward a forceful 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 357. 



reflux wave. The sphygmogram of the ventricular venous pulse 
(Fig. 133) shows an unnaturally high and blunt ventricular wave 
(v) synchronous with the midphase or late phase of systole, as indi- 
cated by the comparable carotid tracing. Pari passu with progres- 
sive enfeeblement of the right auricle, this fl-wave becomes more 
and more conspicuous, encroaches upon the gradually diminishing 
curves of the a- wave, and finally replaces them completely. Thus, 
a prominent ventricular wave indicates not only tricuspid leakage 
and auricular hypertension, but also compensatory hypertrophy 




Fig. 133. — ;Sphygmogram of the ventricular or systolic type of venous pulse. (Tracing 
by Dr. G. Bachmann.) 

of the right ventricle, and, therefore, it may be considered a good 
index of the nutrition and the pumping power of the ventricle. 
With a loss of this efficiency, the v-wave correspondingly diminishes, 
and, should advanced myocardial degeneration exist, this undulation 
does not appear on the tracing. 

The Penetrating Venous Pulse. — A penetrating or centripetal venous 
pidse is sometimes demonstrable in the small veins of the extremities 
under conditions that allow the transmission of the arterial pulse 
to the venules. This type of pulse occurs most frequently, if not 
solely, in connection with Quincke's capillary pulse, of which it is 
merely an exaggeration, since the venous pulse depends upon a 
systolic arterial impact of sufficient force not only to jog the blood- 
columns within the capillaries, but also to penetrate the diminutive 
veins beyond them. Obviously, the penetrating venous pulse is a 
product of the pulsus celer, and hence it is to be looked for chiefly 
as a sign of aortic leakage, and also in states of extreme vascular 
relaxation (v. s.). 



358 PHYSICAL DIAGNOSIS 

PERCUSSION 

The beginner will be likely to regard cardiac percussion as a 
somewhat bewildering procedure, and even the experienced clinician 
cannot always rely upon its findings as incontestable. A cultivated 
ear, a sensitive pleximeter finger, and the strict adherence to a routine 
technic are essential for the best results, however experienced the 
examiner may be. Presupposing these preliminaries, it is possible, 
by percussion of the precordial region, to determine the situation, 
the size, and the shape of the heart; to detect the presence of an 
effusion within the pericardial sac; and to fix the position of the left 
anterior pulmonary border. 

The Areas of Cardiac Flatness and Dulness. — Normally, 
two precordial regions, affording respectively flatness and dulness, 
can be distinguished by careful percussion of the heart: an inner 
area of flatness, over that part of the heart within the cardiac in- 
cisura of the left lung and lying directly against the chest-wall, 
without the interposition of pulmonary tissue; and an outer area of 
dulness, overlying that part of the heart separated from the chest- 
wall by the intervening pulmonary borders (Fig. 134). Of these 
two regions, which together compose the total precordial area, the 
inner is ordinarily designated as the area of absolute or superficial 
dulness, and the outer as that of relative or deep dulness, than 
which terms the words flatness and dulness seem clearer and more 
definite acoustically. The anatomic relations of these two zones 
are shown by Fig. 135. 

The area of cardiac flatness is a triangular space overlying the 
right ventricle, and affording, on gentle percussion, flatness or abso- 
lute dulness, with decided resistance to the pleximeter ringer. The 
right border (perpendicular) of this triangle follows the left sternal 
border from the fourth to the sixth costal cartilage; the left border 
(hypotenuse) extends from the fourth left chondrosternal articulation 
to the junction of the left parasternal line and the upper border of 
the sixth rib (about \ inch, or 1.25 cm. within the apex); and the 
lower border (base) runs from this point somewhat obliquely upward 
to join the lowest extremity of the right border, at the sixth chondro- 
sternal junction. The base of the triangular flatness, inasmuch as 
it blends with hepatic flatness, cannot be mapped out by ordinary 
finger percussion. The principal object of mapping out the area 
of cardiac flatness is to decide if the left lung be -either cirrhotic or 
emphysematous, since pulmonary retraction extends, and pulmonary 
overdistention restricts, this inner cardiac zone, while its extent is 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 359 



not necessarily altered by changes in the size, position, and shape 
of the heart. 

The area of cardiac dulness, surrounding the triangle of flatness, 
approximately corresponds to the anterior aspect of the heart, being 
the surface outline chiefly of the right ventricle, and, to a minor extent, 
of the right auricle and left ventricle. Over this area strong percus- 
sion affords dulness blended with pulmonary resonance, and attended 
by a correspondingly modified sense of resistance. From the cardiac 
base line (upper border of third rib) the outer dulness of the heart 



Cardiohepatic angle 
Hepatic dulness 
Hepatic flatness — ~ 




Cardiac dulness 
— Cardiac flatness 



Fig. 134. — Percussion areas of cardiac flatness and dulness. 

extends vertically along the right sternal border 1 to the sixth costal 
cartilage, whence it follows the lower border of the heart to the apex, 
and then curves upward, with an external convexity, to join the base 
line at the left sternal border. The area thus mapped out extends 
roughly -f inch (i.g cm.) beyond the triangle of cardiac flatness, 
except at the lower border, where both have the same limit; it is 
impracticable to try to delimit the upper border from the area of 

1 " In many cases the whole extent of the sternum furnishes such a loud 
tone that the deep cardiac dulness is really limited by the left sternal border " 
(Sahli). 



S6o 



PHYSICAL DIAGNOSIS 



vascular dulness. The junction of the horizontal limit of hepatic 
dulness with the right lateral line of cardiac dulness forms an approxi- 
mate right angle of resonance in the fifth right intercostal space, 
close to the sternal border — the cardiohepatic angle of Ebstein. 

Postural influences account for alterations in the extent of the lat- 
eral cardiac borders, the right border, when the subject changes 
from recumbency to the erect posture, shifting outward about 
half an inch (1.25 cm.), while the left border extends similarly for 
half this distance. It is obvious that these postural differences, 
relating to the normal heart, are greatly exaggerated when dealing 
with an enlarged heart. 

The area of vascular dulness, overlying chiefly the aorta and the 
superior cava, extends between the sternal margins from the cardiac 
base line to the lower borders of the first costal cartilages. Nor- 
mally, this area affords, on moderately strong percussion, impaired 
osteal resonance that shades off almost imperceptibly as Louis' 
angle is approached. Extension of the vascular area, especially 
upward and toward the right, with or without definite flatness over 



Dull 



Flat 



Dull 




Fig. 135. — Transverse section of the thorax, illustrating the anatomic relations of 
the areas of cardiac dulness and flatness. 



the sternum, is one of the earliest and most valuable signs of 
aneurism of the aortic arch and of extensive dilatation of this vessel. 
Methods and Technic. — With the patient either semirecumbent 
or lying flat on the back, the examiner percusses from frank pul- 
monary resonance toward the precordia, carefully noting the tonal 
modifications and changes in resistance that occur when the outer 
and inner cardiac zones come within the percussion sphere. For 
clinical purposes it is generally sufficient to outline the upper level 
of the heart at the left of the sternum, and to mark its two lateral 
limits on either side of this bone. This is usually done by ordinary 
finger percussion, though auscultatory percussion perhaps gives 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 36 1 

more dependable results and sometimes enables one to determine 
the upper (cardiovascular) and the lower (cardiohepatic) levels. 
Advocates of instrumental percussion claim that with an ivory or 
a vulcanite pleximeter all the cardiac boundaries can be accurately 
mapped out. 

In outlining cardiac dulness percussion is carried downward from 
the left infraclavicular region along the sternal and parasternal 
lines, to fix the upper border; horizontally inward from the left axilla 
along the third, fourth, and fifth interspaces, to designate the left 
border, which, at the level of the fourth rib, lies from ij to 2 inches 
(3.8 to 5.08 cm.) from the midsternal line; and, finally, from a 
resonant point in the right mammary region inward along the 
third, fourth, and fifth interspaces, to indicate the right border, 
lying 3§ inches (8.75 cm.) from the midsternal line, at the level of 
the fourth rib. The points along these percussion lines corre- 
sponding to the dulling of pulmonary resonance are then joined by 
a continuous line, to represent the total outer dulness of the heart, 
the upper sternal base line and the lower border being connected 
arbitrarily. 

In mapping out the area of cardiac flatness the percussion strokes 
are directed from above downward midway between the sternal and 
parasternal lines; inward on the right side, at the levels of the fourth 
and fifth costal cartilages; and inward on the left side along the 
fourth and fifth interspaces. Proceeding in this manner, the per- 
cussion sound successively affords resonance, dulness, and flatness 
as the lungs, the lung-covered heart, and the exposed heart are 
traversed, in the order given. 

The foregoing technic, which meets all ordinary demands, will reveal 
any undue extension of the lateral and lower left borders of the heart, 
indicative of this organ's enlargement. The accurate delimitation 
of the outline of a normal-sized heart is next to a physical impossi- 
bility — aside from the " personal equation," the continual move- 
ments of the heart and the depth of its outer margin, the individual 
differences in the thickness of the pulmonary borders, and the sonor- 
ous vibrations of the sternum make the attempt futile, in so far as 
the exact correspondence of the percussion outline to fixed anatomic 
landmarks is concerned. The same comment applies to percussion 
of the vascular area, the extension of which is betrayed chiefly by 
unnatural parasternal dulness. The diagram on the opposite page 
(Fig. 135) shows the anatomic difficulties that beset precise delimita- 
tion of the cardiovascular regions. 

Increased Cardiac Dulness. — Extension of the area of cardiac 
dulness depends upon both intrinsic and extrinsic factors, the former 



362 PHYSICAL DIAGNOSIS 

relating to changes in the heart itself and in the pericardium, and 
the latter to traction and pressure exerted upon the heart by adjacent 
structures. 

A general increase in the area of cardiac dulness, particularly of 
the transverse diameter, is encountered in bilateral ventricular hyper- 
trophy and dilatation, and a similar change is sometimes noted in 
moderate-sized pericardial effusion. Increased flatness, forming 
a roughly pyramidal or pear-shaped figure, is symptomatic of an 
extensive effusion into the pericardium; the apex of such a flat pyra- 
mid points upward, perhaps as high as the second interspace; the 
borders are sharply defined from the surrounding lung resonance; 
the boundaries usually extend laterally when the patient leans forward; 
and the cardiac apex is partly or completely obliterated. Extension 
of the normal area of the heart, without actual enlargement, may 
be due to cirrhotic shrinkage of the left lung, or to a neoplasm or 
an aneurism crowding the heart forward against the chest-wall. 

Increase of cardiac dulness to the right is suggestive of hypertrophy 
and dilatation of the right heart, less commonly of moderate peri- 
cardial effusion, or of a greatly distended inferior vena cava. Such 
conditions dull the normal pulmonary resonance of Ebstein's cardio- 
hepatic angle in the fifth right interspace at the sternal edge. 

Increase of cardiac dulness to the left and downward is character- 
istic of left ventricular hypertrophy and dilatation, a lesion which also 
displaces the apex-beat in the same direction, and modifies its force 
according to the nature of the predominant myocardial condition. 

Decreased Cardiac Dulness. — Atrophy of the heart accounts 
for a corresponding contraction of the surface boundaries of the 
organ, and in that rare lesion, pneumopericardium, the area of cardiac 
flatness is replaced by the tympany of the air-distended pericardial 
sac. In phthisis it is common to find the size of the heart smaller 
than normal, and Adler has described a form of congenital micro- 
cardia in hypochondriacal subjects. More commonly, how- 
ever, diminution of the area of flatness is referable to some extra- 
cardiac cause — emphysema, which envelops the heart with a hyper- 
resonant covering of overdistended lung ; pleural adhesions, whereby 
a resonant pulmonary border may be permanently anchored di- 
rectly in front of the heart; left-sided pneumothorax, whose clear 
tympany encroaches upon the triangle of cardiac flatness and per- 
haps displaces it toward the right. Simple gaseous distention of 
the stomach diminishes the flatness of the heart from below upward 
and, as W. Gordon has pointed out, gastric cancer reduces or even 
obliterates the cardiac flatness, in the recumbent position. 

Recent £-ray studies have shown that the size of the normal 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 363 

heart diminishes after muscular exercise, and is not increased by a 
state of temporary dilatation, as formerly believed. This fact has 
been proved conclusively by the researches of Nicolai, Zuntz, and 
numerous other investigators, who corroborate the pioneer work 
of Moritz on this subject. Of 100 subjects examined teleront- 
genographically by Williamson, the vast majority of normal hearts 
responded to any exercise within their power by definite contrac- 
tion, and even in pathologic hearts the same tendency was noted 
in one-half of the cases examined. 

Displacement of the cardiac area is determined by the position of 
the heart's impulse, rather than by percussing out the dislocated 
area, and the circumstances under which the various cardiac dis- 
placements occur have been referred to at length under the Apex- 
beat. (See p. 325.) 

AUSCULTATION 

By auscultation of the precordial area one judges the intensity, 
quality, and rhythm of the cardiac tones, and determines the presence 
or absence of unnatural adventitious sounds of endocardial and 
pericardial origin. Like other methods of examination, auscultation 
of the heart must be carried out systematically, in order to afford 
the best results, the-four different valve areas being studied in regular 
order so as to compare and correlate the various sounds. Thus, 
the mitral sounds are first investigated, and then the aortic, to ascer- 
tain the auscultatory findings relating to the left ventricle; while the 
sounds afforded by the tricuspid and the pulmonic valves are the 
key to similar signs pertaining to the right ventricle. 

The heart-sounds should be auscultated with the patient in both 
the recumbent and the upright position, for posture has a decided 
modifying effect on certain heart-sounds, notably on endocardial 
murmurs, some of which can be made to appear and to vanish, 
virtually at will, by changing the subject's posture. (C/. p. 324.) 

The advantages of the binaural and the monaural stethoscope 
in cardiac auscultation, and the application thereto of the trans- 
manual method of auscultation have been pointed out elsewhere. 
(See p. 28.) Abrahams suggests the use of stethoscopic auscul- 
tation of the voice sounds outside the upper and lateral cardiac 
boundaries as a substitute for percussion in delimiting these 
lines. The examiner, having placed the stethoscope in the inter- 
spaces over the pulmonary tissue several inches outside the con- 
ventional cardiac limits, auscultates while the subject repeats 
"ninety-nine" in a low voice, and, moving the bell of the instru- 
ment toward the heart, marks the several points at which the 



364 PHYSICAL DIAGNOSIS 

2 

pulmonary fremitus becomes inaudible and the sounds become 
extrastethoscopic. These points of lost vibration, which mark 
the transition from sound-conducting lung to non-conducting 
heart, are joined later with a line to represent the outer boundaries 
of the entire cardiac area (v. s.). 

Auscultatory or Valve Areas. — Four different auscultatory 
areas, corresponding to the puncta maxima of the separate valvu- 
lar sounds, are made use of in cardiac auscultation: the mitral, 
the tricuspid, the aortic, and the pulmonic (Fig. 136). These areas 

, represent the points upon the 
#^jj^ precordia at which the sounds 

M of the corresponding valves 

3Cr are most distinctly audible, 

n J| and they do not overlie the 

anatomic seats of the valves, 
all of which lie in the imme- 
diate neighborhood of the 
third left chondrosternal artic- 
ulation. (See p. 318.) 
-%y\ f§pi^ The mitral area is indi- 

1 : S cated by a circle about 1 inch 

(Q\ (2.5 cm.) in diameter, centered 

at the cardiac apex, or at 
that point where the apical 
thrust of the heart impinges 
against the chest-wall during 
systole. 

The tricuspid area overlies 
the lower end and right half 

Fig. 136.— Auscultatory areas of the cardiac f the Sternum, from the fourth 

to the sixth or seventh costal 
cartilages, in which situation the right ventricle and the parietes 
are in close relation. 

The aortic area is situated at the sternal end of the second right 
intercostal space and costal cartilage (aortic cartilage), where the 
aorta and the aortic valve approach nearest to the surface of the 
chest. 

The pulmonic area is at the sternal end of the second left inter- 
costal space, over the most superficial projection of the pulmonary 
artery and valve. 

The Normal Cardiac Sounds. — Each beat of the heart is accom- 
panied by two sounds, audible in the precordial area as tones having 
a distinctive grade of intensity and a sui generis quality. These 




EXAMINATION OF THE CARDIOVASCULAR SYSTEM 365 

tones, which occur rhythmically and bear a definite relation to the 
events of the cardiac cycle, may be represented by the monosyllables 
lup-dftp} The //?/>-element is the first sound of the heart, and is 
synchronous with ventricular systole, through about two-thirds of 
which phase it persists, ending in a gradual diminuendo. The 
J/?/>-element, following the first sound after a brief interval, is the 
second sound of the heart, and coincides with the closure of the 
semilunar valves and the beginning of ventricular diastole; it is 
relatively short, sharp, and of abrupt termination, and is separated 
from the succeeding //7^-sound by a comparatively long interval of 
silence (Fig. 137). Phonetically, the rhythmic succession of the 



Fig. 137. — The normal cardiac sounds. 

two sounds may be sketched: lup-dup — lup-dup — lup-dup, the 
interval between the two sound elements representing the short 
pause, and that between their recurrence the long pause, of the 
cardiac cycle. The diagram on page 320 shows the relation between 
the normal sounds of the heart and its cyclic phases. 

The first sound, synchronous with the cardiac impulse and relatively 
more intense at the apex than at the base of the heart, is a musculo- 
valvular tone, due partly to the muscular rumble of the contracting 
ventricles, and partly to the sudden vibratory tension of the mitral 
and tricuspid valves at the time of their closure. The first factor 
accounts for the dull, prolonged, booming quality of the sound 
(muscular tone), and the second explains its tinge of high-pitched 
sharpness (valvular tone). Under normal conditions the character 
of the first sound is subject to individual variations, being, for exam- 
ple, shorter, higher pitched, and more valvular in slim, spare sub- 
jects than in those whose covering of muscle and fat is abundant. 

The mitral first sound is more prolonged and a trifle lower in 

pitch than the tricuspid — a difference that can be detected by careful 

auscultation of the separate ventricular elements of the sound at the 

*With tolerable constancy it is also possible to distinguish, in perfectly 
healthv persons, a third cardiac sound, audible at the apex as a faint tone 
directly after the dup of the .second sound, or during the beginning of the dias- 
tolic period. Thayer suggests that this so-called "third heart-sound " may 
be caused bv sudden tension of the mitral and possibly the tricuspid valve oc- 
curring during the protodiastolic phase. The sound, which is especially clear 
in the voung, is sometimes accompanied by a synchronous impulse which may 
be both visible and palpable, is intensified 'by left lateral recumbencv and dur- 
ing expiration, and is commonest in subjects with a slow pulse. 



366 PHYSICAL DIAGNOSIS 

mitral and the tricuspid areas. This difference is especially notic- 
able in early life; it is to be explained possibly by assuming an intrin- 
sically louder mitral sound, certainly by the fact that the lung between 
the apex of the left ventricle is too thin to affect the sound-waves 
arising within this chamber, while over the right ventricle it is thick 
enough to dampen the sound therein produced. 

The second sound, caused by the closure of the aortic and pul- 
monic semilunar valves, totally lacks muscular tone, and is of a 
purely valvular character; normally, it is louder at the base than at 
the apex. In the young the pulmonic second sound is louder 
and higher pitched than the aortic; in middle life the intensity of 
the two sounds does not differ materially; and in advanced age the 
aortic element is the more striking. The gradual increase in the 
intensity of the aortic second sound is doubtless to be referred to the 
progressive rise in the aortic blood-pressure incident to maturity and 
to old age. Normally, the aortic tension is higher than the pulmo- 
nary, but this physiologic factor of a relatively louder aortic second 
sound is offset by the deep situation of the aorta and its valve, in 
contrast to the superficial position of the pulmonary artery and its 
valve. 

In the majority of healthy subjects of all ages the cardiac 
sounds above the ensiform cartilage have a peculiar superficial 
scratching or crunching quality intensified by forward inclination 
of the trunk and by lateral decubitus. This sound, called "xiphis- 
ternal crunching" by M. Solis-Cohen, has a resemblance to peri- 
cardial friction, but it is regarded as a purely physiologic sign, 
referable perhaps to tensional changes in the loose areolar tissue 
of the sternopericardial ligament acted upon by the movements 
of the heart, as suggested by Bloomer. 

Changes in the Intensity and Quality of the Cardiac Sounds. — 
The normal intensity, tone, and quality of the heart-sounds are 
variously modified in consequence of numerous factors intrinsically 
active or related to parts acoustically intimate with the heart. 'In 
attempting to judge these variations, due allowance is to be made for 
the influence upon the normal sounds of the muscular and adipose 
development of the subject — the thin-chested and cadaverous have 
relatively louder heart-sounds than the muscular and obese, or than 
the woman with generous breasts. 

The intensity of both sounds is markedly increased in cardiac 
hypertrophy, since in this condition of overdevelopment both the 
muscular and the valvular components of the heart-tones are greatly 
exaggerated (Fig. 138). To a lesser degree the sounds are magni- 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 367 



fied by simple cardiac overstimulation, due, for example, to transient 
mental excitement or to the effect of alcohol, coffee, and like stimu- 
lants; or the change may be incident to one of the cardiac neuroses, 
to Graves' disease, and to the effects of an incipient febrile affection. 
Pulmonary consolidations are capable of conducting the cardiac 



A 


\ 


(V s ) 






^ 



i -a 



^^ 



Fig. 138. — Accentuation of both cardiac sounds. 

sounds with abnormal intensity, while pulmonary fibrosis with 
shrinkage may expose the precordia, and thus make the sounds more 
superficial and apparently louder to the examiner's ear. Surgical 
emphysema of the tissues in front of the heart may greatly amplify 
the cardiac tones (Keats) . 

Intensified cardiac sounds with conspicuous alteration of their 
quality are audible when neighboring structures are so changed as 
to act as a resonating chamber for the normal tones. Thus, it is 
possible for the heart-sounds to be echoed as a loud, metallic, hollow 
ring by a distended stomach or gut, by a large, empty, clean-cut 
phthisical cavity, and by a pneumothorax. 

Fig. 139. — Enfeeblement of both cardiac sounds. 

Both sounds of the heart are enfeebled and muffled in myocarditis, 
in dilatation, and in the cardiac asthenia attending conditions of 
collapse, shock, paralysis, and great debility (Fig. 139). Pleural and 
pericardial effusions and hypertrophic emphysema, by covering the 
apex, also lessen the normal vigor of the sounds. In that rare clinical 
curiosity, pneumopericardium, the sounds are usually far away 
and faint; rarely they are louder than normal, amphoric, and bell- 
like. In high-grade anemic states it is common to hear sharp slap- 
ping cardiac sounds, which, though perhaps louder than in health, 
are, nevertheless, to be interpreted as irritably weak. 

Accentuation of the First Sound at the Apex (Fig. 140). — That 
the first sound at the apex is likely to be exaggerated by nervous 
excitement, by physical exertion, and by flatulence should always 
be recalled in examining a patient for the first time. The turbulent 
character of this sound in the high-strung neurotic person or in the 



3 68 



PHYSICAL DIAGNOSIS 



dyspeptic is not, per se, to be construed as an evidence of disease. 
In ventricular hypertrophy, particularly of the left side, the first sound 
resembles a sustained, booming rumble, which, though often muffled 
and impure, gives one the impression of being more intense than 
normal. In dilatation of this cavity the first sound is short, sharp, 



A \ 



Fig. 140. — Accentuation of the first cardiac sound. 

and high pitched, being not unlike the valvular tone of the second 
sound. A loud, high-pitched, snappy first sound at the apex is an 
important diagnostic sign of mitral stenosis. In incipient myo- 
carditis, in the early stages of the acute febrile diseases, and 
throughout the whole course of the febriculae, the apical first sound 
is commonly more or less accentuated and sharp. 



C rr^ 



Ci^ 



Fig. 141. — Enfeeblement of the first cardiac sound. 



Enfeeblement of the First Sound at the Apex (Fig. 141). — Diminished 
intensity of the apical first sound betrays weakness of the ventricles, 
which in some instances is so marked that the sound is practically 
inaudible. Shock, great anemia, collapse, vagus paresis, extreme 
cardiac dilatation, and myocardial degeneration (as in the typhoid 
state and in various forms of myocarditis) are factors by which the 
normal strength of this sound is modified. In mitral regurgitation 
the first sound is enfeebled, but this is difficult to detect because of 
the associated systolic murmur which partly or wholly masks the ven- 
tricular tone at the apex. 



sv\ 



"V\ 



Fig. 142. — Accentuation of the second cardiac sound. 

Accentuation of the Second Sound at the Base (Fig. 142). The 
character of the aortic and pulmonic second sounds at the base of 
the heart is of the greatest clinical value, since the former reflects 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 369 

the strength of the left ventricle and the latter the vigor of the right 
ventricle. In judging the relative intensity of the two sounds their 
physiologic differences must always be considered in the light of a 
modifying element. Accentuation of the aortic second sound, the 
correlative of an intensified mitral first sound, is a sign of increased 
arterial tension within the aorta and the systemic circulation. This 
may arise from purely normal causes, such as temporary vasomotor 
stimulation, a simple overacting heart, and pregnancy. Or the 
loudness and ringing quality of the sound may depend upon arterial 
sclerosis, aortitis, nephritis, and atheroma, dilatation, or aneurism 
of the aorta. In hypertrophy of the left ventricle with competent 
aortic valve segments a similar accentuation is also audible. Accen- 
tuation of the pulmonic second sound, the basic equivalent of an 
intensified tricuspid first sound, develops in consequence of heightened 
pressure within the pulmonary circulation; it is excited by lesions 
that impede the blood-stream within the lesser circuit, as typical 
examples of which may be named pneumonia, and congestion, emphy- 
sema, and cirrhosis of the lungs. In hypertrophy of the right ven- 
tricle the pulmonic second sound rings loudly so long as the intra- 
ventricular pressure is not high enough to produce a " safety-valve " 
tricuspid leakage (q. v.). 

Enjeeblement of the Second Sound at the Base (Fig. 143). — A 
weak, indistinct aortic second sound commonly results from myo- 
cardial degenerations of varying degrees of intensity, and from general 



IB U 103 



Fig. 14.3. — Enfeeblement of the second cardiac sound. 

vasomotor relaxation, whereby the systemic blood-pressure is lowered; 
it may also be due to profound anemia, as in the posthemorrhagic 
form, involving a transient but real oligemia. In both obstructive 
and regurgitant valvular lesions of the left heart this sound is prone 
to become weak, if not inaudible: in mitral stenosis and in mitral 
regurgitation, because the tension within the aorta is too low to slam 
shut the aortic valve with normal force; in aortic stenosis, in con- 
sequence of the deliberate, noiseless closure of the sclerotic and 
stiff leaflets; and in aortic regurgitation, owing to the extensive 
valvular deformity and to the bruit of the diastolic murmur. Pul- 
monary lesions that impede the return of blood to the left side ot 
the heart also account for a feeble second sound at the aortic car- 
tilage. 

24 



37° 



PHYSICAL DIAGNOSIS 



Weakening of the pulmonic second sound is not a common physical 
sign, for the pressure within the lesser circulation is not so readily 
lowered as it is in the systemic circuit. Enfeeblement of this sound 
invariably supervenes when the right ventricle weakens and dilates, 
and it is, therefore, a distinctive and dependable index of this grave 
accident. Tricuspid regurgitation, when associated with right ven- 
tricular weakness, is the factor of a feeble second sound in the 
pulmonic area. 

Reduplication of the Cardiac Sounds. — Reduplication or 
doubling of the first or the second sound of the heart, less commonly 
of both sounds, is heard under a number of circumstances whose 
direct bearing upon these phenomena is not always clear. Three dis- 
tinct sounds in each cardiac cycle are audible when a single (first or 
second) cardiac tone is reduplicated; four sounds, when the doubling 
affects both tones. If the first sound be reduplicated, the precordial 
sounds may be imitated thus : lurrup-dup — lurrup-dup; if the second 
sound be doubled, the effect will resemble: lup-durrup — lup-durrup. 
Single reduplication is much more common than double, and splitting 
of the second sound more frequent than of the first. 

In certain instances the reduplication simulates the hoof-beats of 
a galloping horse, and hence is termed variously bruit de galop, or 
gallop rhythm, or canter rhythm; in other cases it sounds not unlike 
the double beat of a snare drum — bruit de rappel. In the former, 
the doubled elements are divided by a brief pause; in the latter, they 
occur almost, though not quite, synchronously. 

Reduplication of the first sound is almost invariably heard only 
at or near the apex, being audible at the base of the heart only as a 
rare exception (Fig. 144). It is not a true reduplication, but rather 



Fig. 144. — Reduplication of the first cardiac sound. 



an apparent doubling, the mechanism of which is probably not always 
identical. Asynchronism in the closure of the mitral and tricuspid 
valves, the presence of an obscure presystolic murmur, unduly 
strong auricular action, and vibration of the aortic wall are four 
possible causes of the doubling. 1 Systolic reduplication may be 
met with in mitral disease, in arterial sclerosis, in hypertrophy and 

1 For the many theories of systolic doubling the reader should consult the 
writings of Gibson, Barr, Sansom, Bramwell, Johnson, Hayden, Offenbacher, 
and Guttman. 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 3/1 

structural degenerations of the heart, and in chronic adhesive 
pericarditis. 

Reduplication of the second sound is most commonly heard at the 
base, but also at the apex, and at base and apex coincidentally 
(Fig. 145). Doubling at the base is commonly ascribed to asyn- 
chronous closure of the semilunar leaflets, caused by unequal tension 
in the general and the pulmonary circulations. Owing to this loss 
of balance, systole of the ventricle that must overcome the highest 
tension is delayed, and its semilunar valve closure is correspondingly 
tardy. This type of doubling may occur physiologically, from 
forced, full inspiration; it is pathologic when resulting from lesions 
upsetting the equilibrium of the pulmonary or the systemic circuits. 
Therefore, it may be symptomatic of obstructive lesions of the lungs, 
arterial sclerosis, left-sided valvular defects, myocarditis, hyper- 
trophy, dilatation, and pericardial effusion. Reduplication of the 
second sound, heard at the apex, but not at the base, is apparent, 
rather than actual, and has a very different significance from the 
doubling just mentioned. It is an early and characteristic sign of 
mitral stenosis, and almost constantly develops in advance of the 
presystolic rumble of this lesion. The forcible entrance of the 
auricular blood-column produces a sudden, sharp tension of the 
mitral curtains, and this impact, occurring just after the second 
sound, counterfeits a doubling of the latter. 



Fig. 145. — Reduplication of the second cardiac sound. 

Arhythmia. — Disturbances of the normal rhythm of the heart- 
beat may depend upon structural damage to the cardiac musculature, 
whereby its orderly contractions are interfered with, or they may be 
referable to erratic action of the vagus and sympathetic nerves. The 
former factor rules in the arhythmia attending acute infectious 
processes, valvular disease, acute cardiac dilatation, chronic myocar- 
ditis, and fatty heart, while nervous influences are particularly active 
in the disordered rhythm incident to neuroses, great emotion, intra- 
cranial lesions, gastro-intestinal disturbances, certain toxemias, and 
the action of drugs like digitalis, aconite, and belladonna. 

Simple arhythmia of the heart's action is distinguished by various 
deviations from normal force and rhythm, and a heart thus affected 
may afford a medley of intense and feeble sounds so unequally spaced 



.37 2 PHYSICAL DIAGNOSIS 

and so diverse in other details as to defy comparison and description. 
Cardiac arhythmia reaches a climax in that condition of extreme 
irregularity and palpitation so aptly termed delirium cordis, not 
infrequently met with in advanced valvular and myocardial disease. 
Disordered cardiac contractility may account for the presence of 
alternately loud and feeble heart-sounds, the tactile equivalent of 
this type of arhythmia being a radial pulse whose beats are alter- 
nately strong and weak — the pulsus alternans (q. v.). Rhythmic 
irregularity of the heart is designated as allorrhythmia. 

Intermittence, or the omission of a beat, may be independent of 
simple irregularity, but the two are commonly associated. Genuine 
intermission, due to the actual omission of a ventricular systole, is 
to be distinguished from simulated intermission, wherein the con- 
tractions of the ventricle occur, though too feebly to produce a 
peripheral pulse. (C/. p. 344^ 

Respiratory arhythmia is characterized by a periodic accelera- 
tion of the cardiac rate during inspiration and a slowing of the rate 
during expiration, and is a genuine example of "sinus arhythmia" 
depending upon alterations in the tone of the vagus. In young 
children such an irregularity is peculiarly common with ordinary 
respiratory movements, and hence has been designated by Mack- 
enzie as the "youthful type of arhythmia"; in adolescents and in 
young adults it may be provoked by forced, deep respiration. 
Clinically, respiratory arhythmias are recognized by their restric- 
tion to early life, their direct relationship to respiratory move- 
ments, and the perfect correspondence of the peripheral pulse, 
the precordial impulse, and the cardiac sounds. Sinus arhyth- 
mias of this kind are not of serious import, and are promptly 
abolished by the administration of atropin and by other factors 
of rapid cardiac action, such as pyrexia and muscular exercise. 
They show, on the sphygmogram, virtually no variation of the 
height of the arterial peaks, and on the electrocardiogram no 
disturbance of sequential contractions — merely irregular inci- 
dence of the beats. 

Extrasystolic Arhythmia. — Extrasystoles, or premature contrac- 
tions of the ventricles and the auricles, occur in consequence of 
isolated stimuli arising abruptly in parts of the cardiac musculature 
away from the specialized tissue of the sino-auricular node, where 
the normal contraction waves begin. Thus, with an increased 
irritability of the myocardium as a factor, numerous ectopic con- 
tractions are suddenly excited prematurely in relation to the 
normal systoles, and in consequence disturb the orderly sinus 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM $-]$ 

impulses of the heart. This type of arhythmia is commonest in 
men of advanced age, and in those who show evidences of myo- 
cardial degeneration and of valvular lesions; in many cases there is 
a past history of rheumatism, in others it is associated with a tem- 
perament of nervous unrest, or it may accompany apparently per- 
fect health. The use of tobacco in excess, prolonged and fatiguing 
exercise, arterial hypertension, and digestive disorders are additional 



A * * 


Carotid. 


X v^V_ 


^ 


V 


Cardiac /lpeX> 




Time '/s sec. 






Fig. 146. — Sphygmocardiogram illustrating extrasystolic arhythmia. Asterisks indi- 
cate extrasystoles. (Tracings by Dr. G. Bachmann.) 

provocative causes of premature contractions, which ordinarily 
subside as the result of fever, deliberate apnea, recumbency, and 
moderate muscular exertion. 

The occurrence of ventricular extrasystoles, wherefrom irregu- 
larity, inequality, and intermission of the heart's contractions 
arise, is an exceedingly common factor of disordered rhythm 
(Fig. 146). According to the law of maximal contraction (Marie; 
Bowditch) the heart, when stimulated to contract, does so with 



374 PHYSICAL DIAGNOSIS 

its maximal power, regardless of the strength of the stimulus. 
Furthermore, each contraction thus excited completely exhausts 
for the moment the energizing material of the cardiac tissues 
essential for this act, and until this material again accumu- 
lates in sufficient quantity, fresh stimuli fail to excite a systole. 
Normally, this phase of cardiac excitability, termed the refractory 
period, begins just before the time of systole and persists throughout 
this period, the heart acquiring more and more sensitiveness as 
diastole progresses. Abbreviation of the refractory period and 
premature stimulation of a contraction, whether of physiologic or 
pathologic origin, result in an extrasystole timed soon after the normal 
beat. Should the extrasystolic refractory period overlap the time 
of the next physiologic stimulation, the ventricle, being at this time 
unresponsive, cannot react to the stumulus, and, in consequence, 
does not contract; intermission of a heart-beat therefore occurs. 
Extrasystolic arhythmia may also conform to a regularly intermittent 
type, or allorrhythmia, the superadded contractions occurring in 
groups of two or of three successive beats followed by a pause, 
and producing respectively the bigeminal and the trigeminal pulse. 
This variety of arhythmia is illustrated by the sphygmograms IV 
and V shown on page 348. 

Auricular extr asystoles are regarded as contractions excited by 
abnormal stimuli arising in the structure of the auricles, which, 
fatigued by these aberrant efforts, fail to respond to the immediately 
succeeding normal stimuli originating at the venous mouths. 
Each extrasystole of the auricle, therefore, is followed by a long 
pause, indicating quiescence of both auricles and ventricles, and 
this in turn is followed by the next normal contraction. Both the 
auricular and the ventricular types of extrasystole affect the cardiac 
sounds and the arterial sphygmograms similarly, but the jugular 
tracing of the auricular type clearly shows the premature auricular 
undulation, followed by a ventricular wave ushering in a period of 
passivity before the next normal contraction wave. 

Auriculoventricular extr asystoles, in which the premature con- 
tractions are of nodal origin, are characterized by synchronous or 
almost synchronous contractions of the auricles and ventricles, 
and account for the irregularity known as nodal or a-v rhythm. 
Inasmuch as the contraction impulse is displaced from its normal 
situation at the sino-auricular node to a site in the junctional 
tissue (the a-v node), the normal a-v interval is disturbed, being 
either greatly abbreviated or indeed quite effaced, so that the 
excitatory waves reach the auricles and ventricles at the same in- 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 375 

stant and thus excite synchronous contraction of all four cardiac 
chambers; if the ventricles contract before the auricles, the v-a 
interval is disturbed. To account for this type of arhythmia it is 
assumed that the secondary nodal center initiates contraction 
either because of an abnormally slow sinus rhythm or that it does 
so because its inherent activity is disproportionately enhanced. 
While presenting no definite subjective symptoms, the jugular 
tracing registers an abbreviated as interval, a blending of the as 
waves so as to produce a bifurcated systolic peak, or an appre- 
ciable reversal of the as undulations. In the electrocardiogram 
inversion of the P-wave in leads II and III is the rule, owing to 
the change in the direction of the contraction impulse, and in some 
tracings it is superimposed upon the ventricular undulations R, 
S, T, which otherwise are unaltered. 

Heart-block Arhythmia. — Defective conductivity of the auriculo- 
ventricular muscular bundle produces a type of irregularity charac- 
terized by dissociation of the auricular and ventricular rhythms, 



Fig. 1460. — Electrocardiogram of heart-block. (Tracing by Dr. T. A. Cope.) 

occurring in three principal types: incomplete heart-block, com- 
plete heart-block, and Stokes-Adams' bradycardia, with which is 
to be included a fourth, more rare, variety, sino-auricular block. 

In health the auricular systole takes place one-fifth of a second in 
advance of the ventricular, so that an increase in the time- interval 
between the auricular and ventricular contractions argues disturbed 
conductivity of His' bundle, the function of which is the conduction 
of the auricular contraction waves to the ventricles. When this 
muscular bridge is diseased (as by syphilis, fibrosis, or neoplasm) 
its conductile powers are crippled and a corresponding degree of 
dissociation of the auriculoventricular systoles is produced. Whip- 
ham describes a congenital form of heart-block, ascribed to develop- 
mental defects of the auriculoventricular bundle. 

But the presence of pathologic alterations of the foregoing nature 



376 PHYSICAL DIAGNOSIS 

does not invariably produce heart-block, for the cardiac conducting 
paths may be grossly implicated by disease without any conse- 
quent incoordination of the auriculoventricular contractions, in 
which group of cases the origin of the impulses in Kent's newly 
described node and their transmission along its connecting path- 
way are to be assumed (see p. 321). On the other hand, clinical 
heart-block may occur without pathologic changes in the bundle 
of His, the sino-auricular node, or Tawara's node, and the dis- 
ordered rhythm in instances of this sort is usually referred to pro- 
found vagal depression. 

The electrocardiogram of heart-block (Fig. 146a) shows clearly 
the dissociation of the auricular and ventricular beats, as demon- 
strated by the prolonged P-R intervals, the occasional intermission 
of the R-T waves, and the regular response of the ventricular 
peaks to every second or third auricular wave. 

Incomplete heart-block is said to exist when some, but not all, of the 
auricular waves fail to reach the ventricles, which in consequence 
may occasionally miss a beat at irregular intervals, or may beat 
only with each second, third, or fourth systole of the auricles — a 
2:1, 3:1, or 4:1 auriculoventricular rhythm, as the case may be. 

Complete heart-block, or complete obstruction to the passage of 
the auricular waves, results in absolute dissociation of the auric- 
ular and ventricular systoles, which occur, each having a perfect 
rhythm of its own, independently of each other. 

Stokes-Adams' bradycardia is a syndrome characterized by slow 
ventricular and rapid auricular rates of contraction, attended by 
syncope, epileptiform convulsions, and visible venous pulsations 
in the neck, which ordinarily occur twice or thrice oftener than 
the arterial pulse-beats. 

Although first described by Thomas Spens, in 1 793, this symptom- 
complex was not generally accredited as a clinical entity until 
half a century later, when Stokes' cases, in 1842, with the earlier 
work of Adams, in 1827, invested it with the eponym by which it is 
now known. Stokes-Adams' disease, which may occur at any age, 
is commonest in the male sex, and is attributable to infections such 
as syphilis, rheumatic fever, pneumonia, diphtheria, influenza, 
enteric fever, and to fatal anaphylaxis. Temporary examples of 
complete heart-block are also met with in uremia, and incomplete 
block is readily produced by overdigitalization of a rheumatic 
heart. The pathologic lesions affecting the specialized conducting 
tissues of His' bundle include gumma, neoplasm, atrophy, fibrosis, 
fatty degeneration, ulceration, and calcification; and the damage 
to the heart in general consists of inflammatory changes in the 






EXAMINATION OF THE CARDIOVASCULAR SYSTEM 377 

cardiac muscle and its outer and inner investments, with or without 
sclerosis of the coronary arteries. 

Sino-auriadar block, owing to which there is an entire cessation 
of all cardiac movements, is ascribed to the effect of profound vagal 
influence upon the sinus region of the heart. In this condition the 
electrocardiogram clearly shows the standstill of the heart, by the 
registry* of horizontal streaks just preceding the P-wave and meas- 
uring approximately the distance of two normal contraction waves. 
This dramatic type of arhythmia has been produced experiment- 
ally by firm pressure upon the vagus; clinically, it has been ob- 
served as the result of the toxic action of nicotin, digitalis, and 
salicylic acid. 

Fibrillation Arhythmia. — This type of gross irregularity depends 
upon fibrillation of the auricles, and in the heart so affected a medley 
of new stimuli arising at many different auricular foci replace the 
fundamental sinus rhythm, and produce a persistent disorder of 
cardiac rate. During these confused movements of the auricle 
this chamber remains stationary as a whole in wide diastole, but 
its muscular fibers throughout are extremely active and the wall 
"appears to be alive with movement, and rapid, minute, and con- 
stant twitchings and undulatory movements are observed in a 
multitude of small areas upon its surface" (Lewis). The ven- 
tricular contractions are wholly incoordinate with the auricular 
turmoil, since the regular succession of sinus impulses are mingled 
with a confusion of stimuli which escape from the quivering muscle- 
fibers of the small chambers. According to the conducting proper- 
ties of the a-v bundle, the rate and the rhythm of the ventricular 
contractions vary within wide limits and the arterial pulse is greatly 
disordered. Commonly, the ventricular contractions number 
from 100 to 140 per minute, or they may fall to as low as 40 or 
rise to as high as 200. Originally described by Mackenzie as a 
u nodal rhythm," fibrillation of the auricles is now known to repre- 
sent the birth of independent contraction stimuli in the auricular 
wall away from the sino-auricular node. This form of arhythmia 
is found in fully one-half of all cases of mitral stenosis, and in many 
cases of advanced myocarditis and arterial sclerosis. It may be 
due to hyperthyroidism, to the toxic effects of hydrogen sulphid 
gas, and to the immoderate use of tea, coffee, or tobacco. In the 
exceptional case alteration in the sino-auricular node (inflamma- 
tion, fibrosis, arteriosclerosis) is the underlying pathologic cause. 
Clinically, it underlies the pulsus irregularis perpetuus (q. v.). A 
peculiarity found in most cases of auricular fibrillation is the 



378 PHYSICAL DIAGNOSIS 

wide variation of the maximal and minimal systolic blood-pressure 
figures — a range of from 30 to 60 mm., in Silberberg's experience. 

In the electrocardiogram (Fig. 14.6b) the auricular P-wave is 
replaced by a series of very fine undulations, signifying the auricu- 
lar fibrillations, while the Q-R-S waves are irregularly spaced and 
of variable height, denoting disordered rate and force, respectively. 

Ventricular fibrillation, with gross disorder and incoordinate 
contractions of the musculature, also has been met with, as the 
immediate precursor of death, in angina pectoris, in light chloro- 
form anesthesia, in lightning stroke, and as a sequel to auricular 
fibrillation. Death from this cause is usually sudden, and is pre- 
ceded by disappearance of the radial pulse, and by an electrocardio- 
gram recording complete sequential dissociation of the ventricular 
complexes. 

Drugs such as chloroform, strophanthin, and epinephrin predis- 
pose the heart to ventricular fibrillation, and tracings indicating a 




Fig. 146&. — Electrocardiogram of auricular fibrillation. (Tracing by Dr. T. A. Cope.) 

derangement of intraventricular conductivity should contraindicate 
the use of these drugs. 

Alternation Arhythmia. — This represents an irregularity in the 
force of the succeeding cardiac contractions, without deviation of 
the normal incidence of the beats, and, clinically, accounts for the 
alternating pulse {pulsus alternans), in which the beats, although 
regular in rate and occurrence, are alternately large and small. 
This anomaly depends upon variations in the quantity of blood 
expelled from the left ventricle by its alternately strong and weak 
contractions, and is explained by two different theories: (a) Incom- 
plete ventricular systole, owing to persistence of the refractory 
period in a circumscribed area of the ventricular wall, which fails to 
contract while the other part of the muscle does so with enfeebled 
force (Gaskell; Hering); and (b) general ventricular hyposystole, 
with commensurately weak contractile force (Wenckebach). 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 37Q 

In either event the arterial pulsations are alternately strong and 
weak and the cardiac sounds correspondingly loud and obscure. 
Usually, sphygmocardiographic tracings more clearly show the 
alternating phases of this type of arhythmia than the curves of the 
electrocardiogram (Gravier), and auscultatory sphygmomanometrv 
affords distinctive tonal changes. (See p. 36.) 

Hemisystolic Arhythmia. — This extraordinarily rare disturbance 
is characterized by asynchronous ventricular contractions, or hemi- 
systoles, and is met with in extreme mitral incompetence associated 
with excessive intrapulmonary hypertension. As the result of this 
stress, the right ventricle, gorged with blood and greatly overtaxed, 
makes a double systole, the second contraction representing an 
ineffectual attempt to overcome the circulatory stasis in the pulmonary 
circuit. By this mechanism a double apical first sound is produced, 
the second element of which is loudest over the right ventricle; a 
double apex-beat is also created, but there is only a single arterial 
pulse-wave, inasmuch as the second impulse, being that of the right 
ventricle, cannot influence the systemic blood-stream. 

Another type of hemisystole, excited by excessive digitalization, 
consists of independent contractions, first of the left and then of the 
right ventricle, this peculiarity having been attributed to the com- 
paratively sluggish reaction of the right ventricle to digitalis and to 
the predominant effect of the drug on the left ventricle. 

Prolongation of Diastole. — Prolongation of the second or long 
pause after the second sound converts the physiologic 3-4 time of 
the cardiac cycle into a 4-4 rhythm, the first half of which is occu- 
pied by the first and second sounds and the last half by the dias- 
tolic period of silence. 

In this form of arhythmia both the first and second sounds are 
shorter and higher pitched than normal, and become approximated 
by the shortening of the interval between them, while the diastolic 
pause is sustained through fully one-half the entire cardiac cycle. 
A prolonged diastole is suggestive of advanced myocardial disease, 
owing to which the ventricles, exhausted, ill-nourished, and tottering, 
have become almost too feeble to functionate; the sign may also be 
symptomatic of digitalization. 

Embryocardia. — Unnatural frequency and equidistant spacing of 
the heart's sounds, from prolongation of the short, and abbreviation 
of the long, pause, is termed embryocardia. As the name suggests, 
it resembles the regular beating of the fetal heart, in that the two 
sounds are similar and, since both silences are of equal length, follow 
each other at regular intervals, like the tick-tack of a watch. 

Embryocardia means striking cardiac enfeeblement, by fault of 



380 PHYSICAL DIAGNOSIS 

which the ventricles must labor hard, slowly, and almost fruitlessly 
to expel their contents. The presence of this sign in high-grade arte- 
rial sclerosis, in primary myocarditis, and during the acute infectious 
fevers generally indicates that complete heart failure is not far off. 

An embryocardiac tick-tack may also be associated with simple 
tachycardia, in which event it is to be referred to a shortening of the 
long pause. Occurring under such a circumstance, the sign is not 
of grave import. 

Pendulum Rhythm. — This consists of a succession of uniform car- 
diac tones, evenly spaced, equally intense, and not unduly accelerated, 
in consequence of which peculiarities the regular swing of a pendulum 
is more or less faithfully reproduced by the heart's two sounds. 
This anomaly of rhythm is met with in conditions of arterial hyper- 
tension wherein ventricular systole is prolonged and the second 
sound correspondingly delayed, at the expense of the long pause. 

ADVENTITIOUS SOUNDS 

The normal cardiac sounds, in addition to undergoing rhythmic 
and tonal modifications, are also attended, if not wholly replaced, 
by certain superadded, adventitious sounds of pathologic significance, 
generated within the cardiac chambers and the blood-vessels, between 
the pericardial surfaces, and in the pulmonary structures contiguous 
to the heart. These abnormal sounds, for simplicity's sake, may be 








Systole. Diastole. 

Fig. 147. — Mechanism of normal cardiac systole and diastole. 

grouped as — (a) endocardial; (b) exocardial; and (c) vascular. Endo- 
cardial murmurs, or bruits, are of two principal types, organic and 
functional, the former arising from unalterable structural defects 
of the cardiac valves and orifices, and the latter depending upon 
myocardial enfeeblement and upon changes in the composition of 
the blood. Exocardial sounds comprise the dry rub of pericardial 
friction, the splash of the pericardial succussion sound, and the whiff 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 



38l 



of the cardiopulmonarymurmur ; other extracardiac sounds, primarily 
of pleural and pulmonary origin, include pleuropericardial friction 
and cardiopneumatic rales, the mechanism and meaning of which 
have been explained in another place. (See p. T70 etseq.) Vascular 
adventitious sounds are classified as either arterial or venous, according 
to their seat of origin, and of these sounds, the aneurismal bruit and 
the venous hum are the most important clinical examples. 

ENDOCARDIAL MURMURS 

Organic Murmurs. — No sound whatever, save the I ftp of the 
first, and the dfip of the second, cardiac tone, 1 attends the passage of 
blood through the normal heart, since a column of blood coursing, 
at a normal velocity, through healthy endocardiac orifices and 
chambers does so without the formation of the current oscillations 
essential for the generation of murmurs. In other words, a normal 
endocardiac circulation is comparable, physically, to the flow of fluid 
through a tube of uniform caliber, and having smooth walls separated 
from the current by a film of liquid attached to them by the force of 
adhesion; under such conditions the smooth, uniform, silent flow of 
the fluid is assured. When, on the other hand, structural deformi- 
ties of the valves and orifices exist, the blood-stream is churned into 



Stenotic. 



Regurgitant. 





Mechanism of stenotic and regurgitant murmurs. 



sonorous vibrations, just as fluid passing through a tube swirls about 
and is hurled into tiny jets should it be forced through a constriction 
of the tube's lumen into an expanded portion beyond. An orifice 
organically contracted and therefore obstructing the onward move- 
ment of the blood-stream (stenosis), or an opening deformed so as to 
allow the blood to leak backward (regurgitation) results, in either 
accident, in the passage of the stream into a larger cavity, already 
containing blood, and in consequence blood eddies and vibratory jets 
J Practically, the so-called " third heart-sound," referred to on page 365, 
can be disregarded in routine examinations. 



3 82 



PHYSICAL DIAGNOSIS 



termed fluid veins (Savart's mines fluides) are produced (Fig. 148). 
These sonorous vibrations are conducted, with variable intensity, by the 
cardiac muscle and thoracic parietes to the surface of the chest, where 
they are audible as murmurs {bruit; souffle) and palpable as thrills. 
Inasmuch as a sluggish current of blood is not readily thrown into 
sonorous vibrations, despite the existence of deformed orifices and 
valves, the blood-stream must attain a certain degree of velocity in 
order to generate audible murmurs, in view of which the intensity 
of a given murmur indicates the condition of the circulatory force 
and does not, per se, denote the extent or gravity of an endocardial 
lesion. To some extent blood viscosity bears upon the production 
of murmurs, both organic and functional, since hypoviscosity and 





Systolic 



Diastolic 





Presystolic 



Fig. 149. — The rhythm or time of murmurs. 



undue dilution of the blood-mass favor the creation of vibrations 
therein. Matsuo finds that anemic murmurs, whose intensity is 
inversely proportional to the blood's viscosity value, disappear 
when this figure exceeds 3.0. 

Clinical Attributes of Murmurs. — Having detected a murmur, 
it is next in order to determine its relation to the events of the cardiac 
cycle, its point of maximum precordial intensity and lines of trans- 
mission therefrom, and its quality, intensity, and other tonal charac- 
teristics. By this sort of analysis one attempts to decide whether 
the murmur is simply a functional accident or is a sign of endocardial 
disease, and if the latter be the finding, to discover the anatomic site, 
nature, and extent of the lesion, as well at its effect upon the structure 
and adequacy of the heart. In this inquiry the foregoing data are 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 383 

invariably to be correlated with signs relating to the size and position 
of the heart, to the character of the cardiac tones audible at the four 
valve areas, and to the condition of the arterial and venous circula- 
tions. 

The Rhythm of Murmurs. — Endocardial murmurs correspond 
definitely to the events of the cardiac cycle, and occur during ven- 
tricular systole, ventricular diastole, and auricular systole (Fig. 149). 
The ventricular systole and diastole are taken as the clinical time- 
criteria of murmurs, those occurring with systole, accompanying or 
replacing the first sound, being termed systolic, those coincident 
with diastole, blending with or masking the second sound, being 
known as diastolic; and those audible immediately before systole 
being called presystolic. A post-systolic murmur is audible toward 
the end of systole; a protodiastolic murmur occurs in the earliest part 
of diastole, directly after the first sound; and a mid-diastolic mumur 
corresponds to the middle of the diastolic period. 

Murmurs are timed by determining their relation to the sounds 
of the heart, the visible apex-beat, or the palpable carotid pulsa- 
tion; the radial pulse is not a correct index of ventricular systole, than 
which the pulse-wave at the wrist is appreciably later. 

Puncta Maxima and Transmission of Murmurs. — An organic 
murmur is usually heard most distinctly over the precordial valve 
area corresponding to its seat of production, this site being known as 
the punctum maximum, or point of maximum intensity. Further- 
more, if audible beyond this limit, a murmur tends to be conducted 
selectively along a restricted path termed its line of transmission, or 
area of propagation. The puncta maxima and transmission line? 
of different murmurs will be considered in detail later, but in general 
terms it may be here stated that the former are situated where the 
murmurous orifice lies closest, acoustically, to the surface of the 
thorax, and that the course of the latter is determined both by the 
direction of the blood-current and by the conducting properties of 
the structures lying between the source of the vibrations and the 
chest-piece of the examiner's stethoscope. The initial intensity of 
the bruit, its quality and pitch, and the velocity of the blood-stream 
are also to be taken into account as determining factors of a murmur's 
extraprecordial transmission. 

The Intensity and Quality oj Murmurs. — Like the normal heart 
sounds, the distinctness of murmurs is modified by posture, as 
well as by the conducting properties of the thorax and contiguous 
parts. The acoustic characters and intensity of a murmur vary 
greatly, depending as they do upon the force of the blood-current 
and upon the extent and nature of the underlying lesion, the gravity 



384 PHYSICAL DIAGNOSIS 

of which can by no means be judged by criteria such as loudness and 
tonal attributes. However, generally speaking, a loud murmur 
means that the heart is well nourished and acting adequately, while, 
on the other hand, a feeble murmur suggests that the heart is weak, 
if not failing. This dictum is especially true when applied to an 
instance in which a murmur, once loud, bellows-like, and accom- 
panied by a thrill, dwindles to a mere whiff, unaccompanied by the 
slightest tactile vibrations. 

Progressive increase in the intensity of a murmur generally implies 
that the cardiac strength is correspondingly improved. Some 
murmurs are so loud as to be heard distinctly by the patient, and 
others are so intense that they can be recognized by a bystander. 
A systolic or a diastolic murmur may simply blend with the first 
or second sound of the heart, and thus modify its normal quality, 
or it may be so loud as totally to obscure it, and the greater this 
replacement of the physiologic heart-sounds by the murmur, the 
more extensive the valve defect is likely to be. Thus, a distinct first 
sound plus a systolic murmur at the apex means that the mitral valve 
is not so crippled that it cannot close, though it may do so imperfectly; 
and, similarly, a persistent second sound with a diastolic murmur 
in the aortic area shows that the competency of the aortic leaflets 
is not totally abolished. 

With reference to quality and pitch, a murmur may be described 
as soft, distant, and blowing; or rough, harsh, filing, and rasping; 
or rumbling, churning, and blubbering. Such adjectives as these, 
though by no means certain keys to the source of an endocardial 
murmur, have within certain limits a pertinent clinical bearing. For 
example, the typical mitral presystolic murmur is loud and rumbling 
or blubbering; the systolic mitral murmur, on the contrary, is generally 
soft and quiet and blowing. The systolic aortic murmur is usually 
loud, harsh, and rasping; but the diastolic murmur in this area is 
likely to be distant and subdued, if not, indeed, almost noiseless. 
These facts apply, of course, only to the characteristic case, to which 
exceptions are not uncommon. 

The pitch of a murmur is likewise a most variable quality, being 
low and sonorous in some instances, and high and sharp in others. 
Like other bruits, a musical murmur, or one having a musical 
twang or plaintive tone, may be due to the vibrations of blood- 
eddies, but frequently it is produced by the fenestration of a valve, 
or by the vibrations of thickened chordae tendineae, of a delicate 
thread of fibrin, or of the thin free edge of a valve leaflet. Accord- 
ing to Clement, increased rapidity of the intracardiac blood-flow 
is an important factor of the musical quality. Obviously, a 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 385 

musical murmur, per se, points to no single type of endocardial 
defect. Metallic, amphoric, echoing murmurs arise from the same 
conditions that lend these tonal qualities to the normal heart-sounds, 
the nature of which has already been discussed. 

Peculiarities of quality and pitch are to be carefully noted when 
attempting to differentiate the adventitious sounds afforded by a 
heart tenanted by multiple murmurs, which, though audible at the 
same periods of the cardiac cycle, may differ radically in tone. 

Functional Murmurs. — These bruits, like those of organic 
origin, are due to sonorous vibrations of the circulating blood-stream, 
but, unlike them, they do not depend upon permanent structural 
defects ot the valve mechanism. To this sort of murmurs the 




III. Tricuspid and aortic -■("} O 1. Pulmonic 



II. Mitral 



Fig. 150. — Comparative incidence of functional murmurs of the different valve areas. 

(Cf. Fig. 152.) 

adjectives inorganic, relative, accidental, and hemic are also applied, 
for they are produced by temporary myocardial weakness whereby 
the action of the valves is disarranged, or by dilatation of the conus 
arteriosus, or of the pulmonary artery. Diminished blood density, as 
mentioned above, contributes to the causation of functional murmurs, 
inasmuch as thinning of the blood favors the formation of eddies 
and jets in the circulating stream. Anemia, acute febrile affections, 
and extreme physical exhaustion are the principal factors of func- 
tional murmurs, of which the hemic bruit of chlorosis, the relative 
mitral incompetence of various specific fevers, and the relative 
tricuspid leakage consequent to excessive intrapulmonary tension 
are familiar examples. The presystolic murmur of Flint, met with 



386 PHYSICAL DIAGNOSIS 

in aortic regurgitation, is also, in a certain sense, relative or func- 
tional. (See p. 390.) 

Functional murmurs, in their order of relative frequency, are 
audible at the pulmonic, mitral, tricuspid, and aortic valve areas, 
and in the vast majority of cases are systolic in time, faint and blowing 
in quality, and not conducted far beyond the precordia, though 
within this area they may imitate the transmission lines of organic 
murmurs similarly timed and situated. Functional murmurs are 
not productive of cardiac hypertrophy, of distinctive pulse changes, 
or of consecutive alterations in the basic sounds of the heart. They, 
furthermore, have a transient, fleeting character, for they disappear 
with the removal of their exciting cause — when the blood-count 
improves, after the fever declines, or with the subsidence of the 
heart stress, as the case may be. A functional murmur of purely 
anemic character is ordinarily accompanied by a venous hum 
(q. v.). 

The mechanism of functional murmurs is probably not identical 
in all instances. The pulmonic systolic bruit of anemic states, 
especially chlorosis, is best explained by assuming nutritional weak- 
ness of the myocardium, whereby the conus arteriosus dilates and 
leads to the formation of fluid veins within this portion of the right 
ventricle. The pulmonic area is also the site of an evanescent 
systolic murmur of functional type, occurring in emotional women, 
and termed the "psychic heart murmur." An apical systolic 
murmur, of transient duration, develops in many infectious dis- 
eases in consequence of toxic degeneration of the myocardium. 
This induces stretching of the left ventricle, undue enlargement of 
the mitral ring, and relative shortening of the papillary muscles, 
by fault of which defects the mitral valve fails to close tight during 
the ventricular contraction, and therefore permits the leakage of 
blood from the ventricle into the auricle with each systole (Fig. 151). 
This murmur of "relative" or "accidental" mitral incompetence 
disappears as the patient convalesces and the heart muscle regains 
its normal tone. A murmur of similar mechanism is frequently 
audible at the apex for a very brief period as a consequence of 
physical exercise severe enough to throw undue strain upon the left 
ventricle, by provoking excessive systemic arterial tension. Other 
murmurs, timed similarly, are audible at the apex as the result of 
the formation of audible blood-eddies within a dilated left ventricle, 
without leakage at the mitral orifice. A systolic tricuspid mur- 
mur, of relative type, may arise as the result of valvular dis- 
ease of the left heart, whereby excessive intrapulmonary arte- 
rial tension is set up, thus dilating the right ventricle, and, by 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 387 

enlarging the tricuspid orifice, allowing tricuspid leakage. This 
so-called "safety-valve" murmur is really conservative, in 
that for the time it eases the high pressure within the right ven- 
tricle. (See p. 47 5 Relative tricuspid regurgitation may also 
attend the obstinate obstruction of the pulmonary circuit accom- 
panying certain chronic pulmonary affections. An aortic func- 
tional murmur, if systolic, probably means dilatation of the left 
ventricle without stretching of the aortic ring, or, in other words, 
relative stenosis of the aortic orifice; or transient dilatation of the 
aorta may be the exciting cause of a systolic aortic bruit. The 




Fig. 151. — Mechanism of a functional murmur due to ventricular dilatation: 
I, Normal systolic coaptation of auriculoventricular leaflets; II, incompetence due to 
relative shortening of papillary muscles (chamber elongated); III, incompetence due 
to enlargement of mitral ring (chamber stretched horizontally). 

exceedingly rare diastolic functional murmur audible at the aortic 
area is best explained by assuming it to be the diastolic element 
of a venous hum (q. v.) conducted from the jugular veins down- 
ward into the superior vena cava. 

The differentiation of organic and functional cardiac murmurs is 
generally possible, when all the clinical findings are given due weight, 
though in some instances one must withhold a definite decision, at 
least temporarily. For example, the apical systolic murmur so 
commonly arising in acute rheumatic fever may be symptomatic 
either of endocarditis, myocardial relaxation, or high-grade anemia 



3*Z 



PHYSICAL DIAGNOSIS 



due to the action of the rheumatic toxin, and under such a circum- 
stance one cannot venture an opinion as to the character of the 
murmur until some time has elapsed — sufficient for the murmur to 
disappear, if functional, or for it to become supplemented by corrobo- 
rative signs, if organic. The following table may prove helpful in 
emphasizing the main points of difference between these two types 
of endocardial sounds. 



Time: 

Punctum maximum: 

Transmission: 

Myocardium: 

Pulse: 
Anemia: 
Previous history: 

Basal cardiac sounds: 
Duration: 



Organic. 

Systolic, diastolic, or 
presystolic. 

Varies with site of 
valve lesion. 

Conducted select- 
ively or circum- 
scribed. 

Permanent struc- 
tural changes. 

Often distinctive. 

Not a factor. 

Endocarditis, pro- 
longed muscular 
strain, habitual 
arterial hyper- 
tension. 

Generally show dis- 
tinctive changes. 

Permanent. 



Functional. 

Almost invariably 

systolic. 
Usually at pulmonic 

area. 
Rarely conducted 

beyond precordia. 

Heart not perma- 
nently altered in 
structure. 

No characteristic 
change. 

Frequently an im- 
portant factor. 

No history of organic 
endocardial dis- 



No characteristic 

modifications. 
Transient. 



The Analysis of Murmurs. — The particular defect indicated by 
a given endocardial murmur is ascertained by carefully analyzing 
the several attributes of the sound, and by correlating these data 
with a clear conception of the physical condition of the murmurous 
valve and orifice at the precise moment the sonorous vibrations are 
heard. The four different valve areas and transmission paths 
leading therefrom, therefore, are to be auscultated systematically, 
the examiner meanwhile being guided by these cardinal clues to the 
identity of organic murmurs in general : that at the mitral and tri- 
cuspid areas systolic murmurs mean incompetence, and presystolic 
murmurs, obstruction, of the auriculoventricular orifice; that at the 
aortic and pulmonic areas systolic murmurs indicate obstruction, 
and diastolic murmurs, incompetence, of the arterial outlet of the 
ventricle; and that, as a rule, the bruits of obstruction are intense and 
harsh and clear cut, while those of incompetence are relatively 
feeble and soft and indistinct. 

With these facts in mind, it is convenient to investigate the individ- 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 389 

ual murmurs heard over the precordia according to their relation 
to the four auscultatory sites thereupon. More detailed considera- 



II. Aortic 




— — IV Pulmonic 
III. Tricuspid 



I. Mitral 



Fig. 152. — Comparative incidence of organic murmurs at the different valve areas. 

(C/. Fig. 150.) 




id 



4 



J 



Fig. 153. — The mitral presystolic murmur. 



390 PHYSICAL DIAGNOSIS 

tion, pathologic and clinical, of the individual endocardial lesions 
whereby murmurs are generated is given in Section VI. (See p. 439-) 

Mitral Murmurs. — Murmurs due to lesions of the mitral orifice 
may be of either presystolic or systolic rhythm, the former being 
audible just before the cardiac first sound and indicating obstruction, 
and the latter being synchronous with the first sound and signifying 
incompetence. 

Mitral Presystolic Murmurs. — Mitral stenosis accounts for an 
apical murmur produced by contraction of the left auricle, whereby 
the blood-stream is churned into sonorous vibrations as it is forced 
through a constricted auriculoventricular orifice into the ventricle. 
The rhythm of this murmur corresponds to the end of ventricular 
diastole, at which period the auricle's contractile force and the 
velocity of the blood-current are greatest; less commonly, it occurs 
earlier in the diastolic period, in which case the vibrations depend 
more upon the suction action of the ventricle, which is most powerful 
at the beginning of diastole, than upon the driving force of the auricle. 

The mitral stenotic murmur has its punctum maximum just above 
and within the apex of the heart, is virtually not transmitted thence, 
and is usually accompanied by a distinct apical presystolic thrill 
(Fig. 153). In its typical form the murmur is loud, harsh, and 
ingravescent or crescendo (i. e., gradually increasing in loudness 
as it progresses), and terminates in a sharp, snappy first sound; 
less commonly, it is quiet and soft, as in the "suction force mur- 
mur" of the early phase of diastole. Disappearance of the bruit, 
in that it indicates failing power of the left auricle, is of unfavor- 
able import. Associated signs of mitral obstruction include ac- 
centuation and reduplication of the pulmonic second sound, and 
doubling of the apical second sound. Mitral incompetence and 
obstruction frequently coexist, and ultimately tricuspid incompe- 
tence may supervene, in consequence of the stress imposed upon 
the right ventricle. 

The presystolic Flint murmur of aortic regurgitation is audible in 
the mitral area to which it is practically restricted. For its production 
dilatation of the left ventricle and incompetence of the aortic valve 
are regarded as the essential factors. Owing to the enlargement of 
the ventricular cavity, the anterior cusp of the mitral valve is dis- 
placed, during diastole, from its accustomed mural position, so that 
it projects into the rising tide of blood within the ventricle, and 
consequently becomes the target of two blood-streams coming from 
opposite directions — one regurgitating through a leaky aortic orifice 
and the other issuing (normally) from the mitral opening. By this 
mechanism vibrations of the cusp are set up toward the middle or 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 39 1 



end of diastole, with the generation of a presystolic murmur and 
thrill appreciable at the apex. Flint's murmur lacks the sharp 
apical first sound and the intense ingravescence of the bruit of true 
mitral stenosis, and, moreover, is invariably associated with the 
lesion of aortic regurgitation (q. v.). 

A pericarditic presystolic rumble is occasionally audible at and for 
some distance above the apex, in subjects of plastic pericarditis, 
especially in children. It is most likely that this sound represents 
an auriculosystolic (presystolic) friction-rub, symptomatic of peri- 
cardial adhesion; it is attended by none of the valvular tonal changes 
peculiar to the bruit of mitral stenosis of the organic type (q. v.). 

Mitral Systolic Murmurs. — Mitral regurgitation is responsible for 
the vast majority of all systolic murmurs audible at the apex of the 
heart, the sound betraying incompetence of the left auriculoventric- 
ular orifice, by fault of which each contraction of the left ventricle 
forces a part of its contained blood backward into the left auricle. 
The murmur thus produced blends with or masks the first cardiac 
sound, is commonly of a blow- m 1 

ing character, and from its 
apical punctum maximum is 
transmitted toward the left 
axilla and sometimes to the 
left scapular angle by the 
continuous pathway of con- 
duction formed by the ante- 
rior papillary muscles and the 
ventricular wall (Fig. 154). 
Accentuation of the pulmonic 
second sound is an important 
concomitant sign of this de- 
fect, which, as stated else- 
where, may be due to endo- 
carditic or sclerotic changes, 
or purely to ventricular re- 
laxation, leading to disparity 
between the size of the mitral 
opening and of the valve- 
leaflets that should guard it. 
It is well to remember that 
functional murmurs of mitral regurgitation vanish when the cardiac 
tone improves sufficiently to allow the mitral opening to resume 
its normal diameter, but that murmurs of organic mitral leakage 
are prone to become louder when the force of the heart increases. 








Fig. 154 — The mitral systolic murmur. 



392 



PHYSICAL DIAGNOSIS 



Aortic Murmurs. — Both systolic and diastolic murmurs are 
audible in the aortic area in consequence of disease of the aortic 
valve, those accompanying the first sound indicating obstruction, 
and those synchronous with the second sound, incompetence. Aortic 
svstolic murmurs are more frequently due to sclerotic roughening 
and to dilatation of the aorta than to actual constriction of the orihce, 
while, less commonly, a systolic bruit in the aortic region means 
aneurism. 

Aortic Systolic Murmurs. — True aortic stenosis causes a loud, harsh 
murmur at the aortic cartilage, the sound being transmitted thence 
into the arteries of the neck (Fig. 155^. In typical instances the mur- 
mur is accompanied by a 
coarse thrill and the aortic 
second sound is notably en- 
feebled. Organic narrowing 
of the aortic orihce, at which 
fluid veins are agitated by 
each ventricular systole, ex- 
plains the mechanism of this 
bruit, which rarely exists as an 
isolated lesion. 

rH Aortic roughening, by all 

odds the commonest defect in 
this region, provokes a mur- 
mur of the same rhythm, site, 
and propagation as that of 
genuine stenosis, but it is not 
so frequently associated with 
a thrill, and the aortic second 
sound is loud, clear, and 
ringing. The mechanism of 
Fig- 155-— The aortic svstolic murmur. this bruit is shown bv FisT- 

163. 

Dilatation of the aorta, producing a relative stenosis of the aortic 
orifice, and aneurism of the aortic arch produce systolic aortic mur- 
murs, but in a dilated aorta one expects to find a corresponding area 
of local dulness. as well as an accentuated aortic second sound; 
while in aneurism there is usually no difficulty in discovering dis- 
tinctive evidences of an aneurismal tumor. (See Fig. 163.) 

Aortic Diastolic Murmurs. — Almost invariably these are symp- 
tomatic of aortic regurgitation, whereby the blood-column within 
the aorta falls backward, during ventricular diastole, through an 
organically incompetent orifice, and in so doing sets up a prolonged 




EXAMINATION OF THE CARDIOVASCULAR SYSTEM 393 



soft diastolic murmur, best heard at or below the aortic cartilage, 
and propagated down the sternum and toward the apex or the left 
axilla. The five possible puncta maxima of this murmur are shown 
in the accompanying illustration (Fig. 156). Striking hypertrophy, 
and later dilatation, of the left ventricle develops in consequence of 
this lesion. Relative aortic in- 
competence is recognized by 
the presence of a diastolic 
aortic murmur like that of 
an organic regurgitation, and 
by the absence of the other 
hall-marks of the latter con- 
dition; relative leakage is, 
furthermore, attended by well- 
defined evidences of left ven- 
tricular dilatation and of en- 
largement of the ascending 
portion of the aortic arch. 
That, exceptionally, a diastolic 
anemic bruit may be clearly 
audible in the aortic area is 
a fact worth recalling. 

Tricuspid Murmurs. — The 
tricuspid area affords both pre- 
systolic (stenotic) and systolic 
(regurgitant) murmurs, gener- 
ated by a mechanism directly 

akin to that of corresponding adventitious sounds at the mitral 
orifice. 

Tricuspid Presystolic Murmurs. — The punctum maximum of this 
extremely rare murmur, which never means anything but tricuspid 
obstruction, is at the base of the ensiform cartilage, either near the 
middle or along either border of the sternum, whence it is not con- 
ducted (Fig. 157). The murmur is like that of its mitral counterpart, 
both rhythmically and acoustically, and not uncommonly is accom- 
panied by a presystolic thrill and by enfeeblement of the pulmonic 
second sound of the heart. A tricuspid presystolic murmur ordinarily 
signifies an acquired stenosis, though it may represent a congenital 
defect, either developmental or endocarditic. 

Tricuspid Systolic Murmurs. — A tricuspid systolic murmur may 
be either circumscribed to its punctum maximum or conducted 
therefrom toward the right and upward (Fig. 158). Jugular pul- 
sation of the ventricular or systolic type, hepatic pulsation, and 




Fig. 156. — The aortic diastolic murmur, 



394 



PHYSICAL DIAGNOSIS 




Fig. 158. — The tricuspid systolic murmur. 

weakening of the pulmonic second sound are the important corrobora- 
tive signs of this murmur of tricuspid leakage. This lesion is a very 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 395 

common consequence of right ventricular dilatation, and, with less 
frequency, results from endocarditic deformity of the valve; in a 
limited proportion of cases the murmur is of anemic origin. 

Pulmonic Murmurs. — Organic murmurs having their punctum 
maximum at the pulmonic area, like those of aortic origin, are either 
systolic and stenotic, or diastolic and regurgitant. Such murmurs 
are extraordinarily rare, though, as mentioned above, anemic bruits 
at the pulmonic orifice are not at all uncommon. 

Pulmonic Systolic Murmurs. — Exceptionally, a congenital stenosis 
of the pulmonic orifice exists, to account for a harsh systolic murmur, 




Fig. 159. — The pulmonic systolic murmur. 

most intense at the pulmonic orifice and conducted upward toward 
the clavicle, or, if very intense, spreading over the upper left thoracic 
wall (Fig. 159). Impurity or suppression of the pulmonic second 
sound is a convincing attendant sign, and usually there is cyanosis, 
with more or less definite auscultatory evidences of other congenital 
cardiac defects, notably a pervious interventricular septum. 

In addition to the pulmonic systolic murmurs of anemia and of 
organic constriction, similar sounds may arise from relative stenosis 
of the orifice, created by dilatation of the pulmonary artery imme- 
diately distal to its ventricular mouth, but in this condition the 



396 PHYSICAL DIAGNOSIS 

murmur, which is likely to be soft and quiet, persists only so long as 
the arterial relaxation producing it lasts, and the patient is not 
cyanotic, but debilitated and poorly nourished. 

In auscultating the pulmonic region one must not forget that this 
is the favorite site of a cardiorespiratory murmur, and that here also 
may be heard the bruits of pulmonary artery stenosis, of aneurism, 
and of a patent interventricular septum. .In Section VI. the differen- 
tiation of these puzzling systolic murmurs is dealt with indivi dually. 

Pulmonic Diastolic Murmurs. — Organic pulmonary regurgitation 
is a clinical curiosity giving rise to a diastolic murmur of maximum 



v 




Fig. 160. — The pulmonic diastolic murmur. 

intensity at the pulmonic area, and transmitted thence downward 
and sometimes toward the mitral region (Fig. 160). Also of rare 
occurrence is the diastolic murmur of relative pulmonary incompe- 
tence, or of leakage from stretching of the pulmonic ring incident to 
excessive pressure within the pulmonary artery. Aortic regurgitant 
murmurs are distinguishable only by a process of exclusion from these 
similarly timed murmurs of pulmonary regurgitation (q. v. i). 

Multiple Murmurs. — In organic disease of the endocardium 
two or more murmurs are commonly generated, owing to the 
tendency of endocarditic and sclerotic processes to attack more 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM S97 

than one valve, either simultaneously or consecutively. When they 
correspond to different periods of the cardiac cycle, it is compara- 
tively a simple matter to recognize multiple murmurs by their different 
rhythms, but when the sounds are synchronous, their differentiation 
depends upon the detection of separate puncta maxima and lines of 
transmission, and upon careful study of individual sound-quality 
and other tonal attributes. 

The basal "see-saw" bruit of aortic obstruction and incompetence 
is frequently associated with the apical systolic murmur of mitral 
leakage, and here, aside from differences in tone, rhythm, and maxi- 
mum intensities, one observes three distinct lines of propagation — 
upward into the neck (aortic systolic), downward over the sternum 
(aortic diastolic), and toward the axilla (mitral systolic). A double 
lesion at the mitral orifice produces a rough presystolic apical rumble, 
continuous with a softer and longer systolic murmur, or apparently 
separated from it by a sharp, snappy cardiac first sound. In stenosis 
of both mitral and aortic orifices a presystolic apical and a systolic basal 
murmur are audible, the former being circumscribed at the mitral 
area, and the latter conducted upward. In the combination of 
mitral stenosis and aortic regurgitation the presystolic apical murmur 
of the former defect and the basal diastolic bruit of the latter some- 
times commingle at the apex, but still are separable by their slight 
differences in rhythm and by their decidedly dissimilar quality and 
intensity. Mitral and tricuspid regurgitation in combination create 
a systolic murmur having a double punctum maximum, that of the 
mitral lesion being apical and that of the tricuspid, over the lower 
part of the sternum; between these two intensity points there lies a 
spot where neither murmur is distinct, as demonstrated by the clear 
mitral murmur on its apical side, and by the tricuspid bruit on its 
sternal. 

Apart from differences in their several attributes, multiple murmurs 
must be discriminated largely by associated findings relating to 
structural changes in the cardiac chambers, to the peripheral pulses, 
to the pulmonary circulation, and to sequels such as edema, cyanosis, 
and dyspnea. Auscultatory findings without evidence of this sort 
can give but incomplete data regarding the character of a murmurous 
lesion and its effects upon the cardiovascular system. 

EXOCARDIAL SOUNDS 

Pericardial Friction. — Fibrinous roughening of the pericardial 
surfaces generates a friction-sound the characteristics of which are 
determined by the amount and viscosity of the exudate and by the 



398 PHYSICAL DIAGNOSIS 

force of the cardiac impact. Ordinarily, this friction is most dis- 
tinctly audible along the left sternal border, between the second and 
fourth interspaces (Fig. 161); less commonly it is most intense at 
or near the apex of the heart. The friction-sound is superficial, 
circumscribed, and usually increased by moderate, and perhaps 
obliterated by very forcible, pressure with the stethoscope; it is 
exaggerated when the subject bends forward in the upright position, 
and when he practises Valsalva's manceuver of making forced 
expiratory efforts while the glottis is closed. The rhythm of peri- 
cardial friction is likely to be to-and-fro, corresponding to the move- 
ments of the heart rather than to the clinical cardiac tones with 




Fig. 161. — Punctum maximum of the pericardial friction-sound. 

which it is not exactly synchronous; rarely, the sound is tripled by 
the addition of a presystolic element referable to auricular systole. 
The intensity and quality of a pericardial friction-sound vary greatly, 
according to the pathologic condition existing in the individual case: 
when greatly roughened and very dry pericardial surfaces are rubbed 
together by an overacting heart, the sounds thereby produced are 
loud, rasping, grating, or, indeed, not unlike the creaking of leather; 
when the exudate is moist and buttery, the sounds are fainter, and 
more liquid and clicking in quality. Pericardial friction is a curi- 
ously evanescent, inconstant sign, in that it may be detected one day 
and be absent the next, and may change its punctum maximum from 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 399 

time to time. This point rises as an effusion collects, and should 
the exudate be of sufficient volume entirely to separate the two layers 
of the pericardial sac, the friction-sound may disappear, reappearing 
later, after removal or resorption of the fluid. 

An endocardial murmur, in comparison with pericardial friction, 
is a softer, less superficial sound, accurately corresponding to an 
event of the cardiac cycle, and having a fixed punctum maximum 
and a definite line of transmission or area of localization; furthermore, 
pressure has no effect whatever upon an endocardial bruit, while 
Valsalva's experiment, as a rule, enfeebles it. 

Pleuropericardial friction, though acoustically similar to a peri- 
cardial rub, bears a definite relation to the cardiac impulse and to 
the respiratory movements, is usually most intense at or just outside 
the pulmonary margin bordering on the triangle of cardiac flatness, 
and can be accurately circumscribed to the costal pleura or to the 
pericardial reflection, by noting the effect of full inspiration and 
expiration upon the sound. (See p. 172.) 

Cardiorespiratory Murmurs. — When a segment of air-contain- 
ing lung is compressed between the heart and the chest-wall the 
shock of the cardiac impulse may expel the air from the compressed 
pulmonary structure with sufficient velocity to create a precordial 
murmur, which almost invariably is of systolic rhythm. Such a 
sound is sometimes audible in apparently healthy subjects, especially 
in those whose cardiac action is tumultuous; pathologically, it is 
detected in emphysema, phthisis, external pericarditis, and massive 
pleural effusion, when in these conditions the anterior pulmonary 
margins (particularly the lingula of the left lung) are crowded, com- 
pressed, or adherent in front of the heart so as to receive the full 
force of the cardiac impact. Ordinarily a cardiopulmonary murmur 
resembles a short, subdued puff or whiff of air, but it may be rela- 
tively prolonged, loud, and rasping. It is evanescent in charac- 
ter, restricted to a limited area, intensified by deep inspiration and 
by forward inclination of the trunk, and variously modified by 
cough and by forced respiration. In children murmurs of this 
type account for two- thirds of all endocardial adventitious sounds. 

The origin of diastolic cardiopulmonary murmurs is obscure, and 
probably the mechanism is not always the same. In some in- 
stances rapid aspiration of air into a patch of lung compressed dur- 
ing ventricular systole (Potain) serves as the most logical explana- 
tion, while in others the sound is best explained by assuming that 
adhesions between the lung and the heart or the aorta transmit 
a local suction force to the adherent lung at the period of cardiac 
diastole (Gallavardin ; De Vivo). Should the portion of lung shar- 



400 PHYSICAL DIAGNOSIS 

ing the heart's movements be the seat of an exudate or a transu- 
date, moist cardiopneumatic rales also may be appreciable. (Cf. 
p. 170.) 

Pericardial Succussion Sounds. — The presence of fluid and air 
within the pericardial sac, constituting that very rare clinical entity 
hychopneumoperhardium, gives rise to a melange of splashing, 
tinkling, gurgling, churning sounds audible over the precordia, and 
unmistakably produced by the movements of the heart. These 
sounds, also designated as the metallic gurgle and as the bruit de 
moulin, are sometimes so loud as to be appreciable at a distance from 
the patient; they may have a sharp metallic tone, and partly or 
entirely obscure the normal cardiac tones. Pericardial succussion 
sounds must be distinguished from somewhat similar noises created 
by the impact of the heart against the wall of an adjacent pulmonary 
cavity containing air and liquid, or against a left-sided hydropneu- 
mothorax. 

VASCULAR MURMURS 

Adventitious sounds may be heard over the larger arterial and 
venous trunks, occasionally in health, but more often in pathologic 
conditions. Such murmurs are explained by mural vibrations, by 
the formation of intravascular fluid veins due to a local anomaly of 
the vessel, and by the conduction of a bruit arising at a crippled 
cardiac orifice or within an aneurismal sac. Vascular murmurs may 
be systolic, diastolic, or to-and-fro; continuous or intermittent; and 
sighing, humming, musical, or harsh in quality, according to the 
factors of their production. 

Arterial Murmurs. — If one of the larger superficial arteries 
(for instance, the carotid) be auscultated, the transmitted sounds of 
the heart are audible as dull, muffled systolic and diastolic beats, 
but if pressure with a stethoscope be made, so as to narrow the lumen 
of the vessel, the first sound becomes louder and distinctly murmurish, 
in consequence of the fluid veins formed by the local constriction 
(Fig. 162). By a similar mechanism an artery constricted by adhe- 
sions, by neoplasms, or by enlarged glands is also the seat of a systolic 
bruit. 

A systolic murmur over the carotids is a confirmatory sign of aortic 
stenosis and of atheroma or aneurism of the aortic arch, the sound 
being conducted into the neck from its site of origin by means of the 
blood-current. A systolic murmur over the subclavian artery is 
sometimes audible in the healthy person, when the breath is held 
with the lungs fully inflated; and in apical phthisis a similar murmur 
may occur as the result of compression of the subclavian artery by a 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 401 

fibrous band of adhesions. This subclavian murmur is usually 
most distinct on the left side, in the outer portion of the infraclavicular 
space. Systolic carotid and subclavian murmurs sometimes attend 




Fig. 162. — Mechanism of an arterial pressure murmur. 

high-grade anemias. A diastolic murmur over the carotids and the 
subclavians is generally referable to the conduction of a bruit generated 



Aneurism. 



Atheroma. 





Fig. 163. — Mechanism of arterial murmurs due to aneurism and to atheroma. 

at an incompetent aortic orifice, and a murmur of this sort is audible 

without the slightest compression of the vessel auscultated. 

Duroziez's double murmur over the femoral artery is audible in 

many, but not in all, cases of aortic regurgitation. When the examiner 
26 



402 PHYSICAL DIAGNOSIS 

listens while the chest-piece of the stethoscope rests very lightly upon 
the vessel, a quiet dull systolic thud is heard, indicative of the sudden 
impact of the blood-column against the arterial wall; with moderate 
pressure a somewhat harsh, loud murmur, due to constriction of the 
vessel, replaces the thud first detected; and with still greater pressure, 
carefully graduated so as to produce just the proper degree of arterial 
constriction, the soft diastolic murmur of arterial reflux becomes 
audible. The double sound (normal systolic pressure murmur and 
diastolic reflux bruit) thus developed is designated as Duroziez's 
sign. 

The Venous Hum. — This sound, also known as the bruit de 
diable, nun's murmur, and humming-top murmur, is heard most 
distinctly over the jugular vein at the inner end of the right supra- 
clavicular space, whence, if the sound be intense, it may be transmitted 
to the base of the heart. In auscultation of the jugulars pressure 
upon the vessel must be avoided, for a fictitious murmur may be 
excited should the bell of the stethoscope compress the vessel suffi- 
ciently to constrict it, and thus to produce a fluid vein. Exception- 
ally a venous hum is audible over the courses of the lateral and 
longitudinal sinuses, over the liver, and over the subclavian and 
axillary veins. 

A venous hum sounds not unlike the continuous musical soughing 
of the wind through bare tree-tops, or the aeolian-like buzz of a 
mass of telegraph wires swept by a breeze. More rarely it is fitful, 
intermittent, and blowing in character. The murmur has a rhythmic, 
crescendo quality during forced inspiration, at the time of cardiac 
diastole, and when the patient is in an upright position, for under 
these circumstances the jugular current heartward is accelerated. 
It is intensified when the patient turns the head sharply away from 
the examiner, thus compressing the vein and narrowing its lumen. 
There are several possible factors of the venous hum, none of which 
is a wholly satisfactory explanation of the sign. In anemia the 
hydremia no doubt plays a part, for thin blood flows with 
increased rapidity and tends to form whirling jets; but a more 
important factor in this condition is the nutritional relaxation of 
the walls of the veins, whereby rapid mural vibrations are provoked. 
Chauveau's theory is no longer seriously entertained — that in anemic 
states there is a sort of compensatory contraction of the veins because 
of the oligemia, except where the jugular bulb is attached to the 
cervical fascia, at which point a relative dilatation exists, and here 
fluid veins are formed. Lorrain Smith's work argues a decided 
increase of the blood-mass in chlorosis, and no great diminution of 



EXAMINATION OF THE CARDIOVASCULAR SYSTEM 403 

it in pernicious anemia, and these are the very conditions of which 
venous hums are most frequently symptomatic. 

The venous hum is not necessarily a pathologic sign, since it is 
present occasionally in perfectly healthy persons, especially in the 
young. It usually means anemia, however, and is particularly 
suggestive of chlorosis and of Addisonian anemia. No definite 
relation is apparent between the incidence and the intensity of the 
sign and the grade of the blood deterioration. 

In Graves' disease Snellen has described a systolic murmur, 
elicited by adjusting the chest-piece of the stethoscope over the 
eyeball, with the lids closed. 

THE FUNCTIONAL CAPACITY OF THE HEART 

For the purpose of estimating the functional capacity of the 
heart numerous different methods have been devised, the most 
satisfactory of which are based upon the effects of graduated exer- 
cise upon the cardiovascular system, as indicated by a study of the 
pulse, blood-pressure, and precordial outline (with due attention to 
arhythmia and adventitious sounds) before and after the subject 
is put through a period of active physical strain consisting of volun- 
tary muscular movements or exercises with dumb-bells and the 
horizontal bar. Thus one is enabled, with considerable accuracy, 
to estimate the response of the circulatory system to the strain of 
graduated work, to determine the state of cardiac reserve force, and 
to observe the effects of decompensation. 

A somewhat more elaborate technic, adapted particularly to the 
study of the myocardium and the immediate effects thereon of 
valvular disease, calls for radiographic outlining of the heart before 
and after the administration of a powerful vasoconstrictor drug. 

United States Army Exercise Test. — The pulse-rate and rhythm 
are noted, with the subject in dorsal decubitus, before and after a 
measured amount of exercise consisting of hopping 100 times on one 
foot, and the data thus obtained compared by repeated ausculta- 
tion of the heart for a period of two minutes after the exercise. In 
a normal man the tachycardia thus excited disappears within two 
minutes after the hopping maneuver, but with an impaired myocar- 
dium the high pulse-rate persists ("vagus lag"), along with more or 
less urgent dyspnea, arhythmia, precordial distress, increase in 
the size of the heart, and impure or murmurous cardiac sounds, ac- 
cording to the character of the underlying defect in the individual 
case. To this group of symptoms in recruits failing to pass the 
exercise test Thomas Lewis has applied the term "effort syndrome"; 



404 PHYSICAL DIAGNOSIS 

it includes those formerly labelled D. A. H. (disordered heart action) 
and V. D. H. (valvular heart disease) by the British Army Medical 
Service. S. Calvin Smith, in a compilation of approximately 35,000 
cardiovascular examinations of United States troops, found an 
average pulse-rate of 97.8 before exercise, 128.5 immediately after 
exercise, and 92.6 two minutes later. 

The Pulse Pressure Test. — Normally, after muscular effort both 
blood-pressure and pulse-rate rise, as the result of the compensa- 
tory efforts of the cardiovascular system thus excited. In the 
healthy adult the systolic rise averages 24 mm. and the diastolic 
12 mm. of mercury, the latter figure also indicating the pulse pres- 
sure increase (Middleton), while the pulse-rate runs about 50 beats 
per minute faster than before the exercise (Lowsley). 

Failure to provoke this sort of normal hypertension by moderate 
physical exercise suggests an overtaxed heart, and, as Warfield has 
shown, especially significant is a reading which shows a virtual ob- 
literation of the pulse pressure owing to the approximation of the 
systolic and diastolic figures. Such a finding means serious im- 
pairment of cardiac reserve force (q. v.) , and calls for caution on the 
part of the patient in the matter of exercise and for appropriate 
preventive measures in case prolonged anesthesia and a serious sur- 
gical operation are imperatively demanded. 

The pulse pressure test, as practised by Cashman, is conducted 
by subjecting the patient to moderate exercise, such as walking 
rapidly or the use of dumb-bells, and comparing the pulse-rate and 
systolic, diastolic, and pulse pressures before and after the exercise 
period. The examinations are made with the subject both re- 
cumbent and erect, so as to gage the vasomotor tone, which in con- 
ditions of great debility shows a fall of systolic pressure after chang- 
ing from the recumbent to the erect position, whereas normally a 
compensatory action of the vasomotors prevents hypotension of 
this sort. 

The Epinephrin Test. — The vasoconstriction and consequent 
hypertension induced by a test dose of 1 mg. (.0154 gr.) of epi- 
nephrin imposes extra work upon the heart, which, if sound, shows 
slight if any radioscopic change in its outline an hour later. Within 
this time limit, however, a weakened myocardium shows distinct 
enlargement, due to inherent muscular enfeeblement, to defective 
innervation, or to valvular disease. Of the last named lesions, 
Loeper, who devised this functional test, noted that those affecting 
the mitral and the aortic orifices afford particularly significant shad- 
ows at the apex and the base of the heart respectively. 



SECTION VI 
DISEASES OF THE CARDIOVASCULAR SYSTEM 



PERICARDITIS 



Rheumatic fever is the most common single factor of pericarditis, 
although it is difficult to determine how active a cause it is, owing to 
the wide divergence in the percentages (6 to 75) given by different 
authorities; averaging these data, it seems safe to conclude that from 
30 to 40 per cent, of all cases of rheumatism are attended by peri- 
cardial inflammation. This complication is prone to appear during 
the initial attack of rheumatism, and bears no constant relation to 
the number or intensity of the articular lesions, though it appears to 
be especially frequent when the joints of the upper extremity are 
attacked. Nephritis, gout, diabetes, and the hemorrhagic diseases 
are active exciting causes of pericarditis, which also not uncommonly 
attends pneumonia and scarlatina, and, with less frequency, other 
febrile infections, such as septicemia, erysipelas, variola, diphtheria, 
measles, and enteric fever. A pericardial inflammation may be 
secondary to pleurisy, bronchitis, tonsillitis, myocarditis, or valvular 
disease of the heart (especially aortic regurgitation), or it may develop 
in consequence of some neighboring or remote septic process — costal 
necrosis, mediastinal abscess or neoplasm, empyema, malignant endo- 
carditis, gastric or esophageal ulcer, or peritonitis. Tuberculous 
pericarditis occurs both in a primary form and as a secondary 
process, usually in connection with pleuropulmonary tuberculosis. 
Chorea, even when unaccompanied by arthritic rheumatism, is not 
uncommonly the apparent cause of a pericardial inflammation. 
Traumatic pericarditis, mainly of surgical interest, sometimes super- 
venes in consequence of a penetrating wound of the heart or of a 
violent precordial contusion. 

SOLDIER'S HEART 

The World War has furnished many instances of that symptom- 
complex originally described by J. M. DaCosta (1871) and by 
Harthorne (1864) as the "irritable heart," a condition char- 
405 



406 PHYSICAL DIAGNOSIS 

acterized by nervous and circulatory disturbances met with in 
soldiers during the American Civil War. During the recent con- 
flict an identical group of cases has been studied anew in detail 
by modern methods under different captions, such as "disordered 
action of the heart," the "effort syndrome," "neurocirculatory 
asthenia," "cardiosplanchnic paresis," and "cardiac debility." 

Clinical Pathology. — The pathologic change accounting for the 
syndrome is wholly obscure if from the cases thus far observed the 
influence of rheumatic fever, :horea, and various infectious proc- 
esses is excluded, as it should be. Hyperthyroidism, alone and in 
connection with adrenal insufficiency, has been urged as a causal 
factor, particularly of the circulatory phenomena (James Barr); 
the complex has been attributed to psychoneurotic influences 
(Fraser; Robey; Oppenheimer) ; and to the toxic effects of faulty 
metabolism. The theories that the soldier's heart owed its origin 
to faulty accoutrement and to the effects of the setting up drill on 
the new recruit (Davy) also have proved erroneous. Whatever 
the real nature of the disorder, the fact remains that its develop- 
ment is provoked in all cases by some emotion, excitement, or 
shock insufficient in the healthy man to upset the normal cardiac 
innervation. 

Physical Signs. — Inspection. — Dyspnea is the conspicuous ob- 
jective symptom in fully two-thirds of all cases, and occasionally 
the breathlessness is so aggravated that the orthopneic posture 
must be assumed by the patient. As Hume observes, in many 
instances the dyspnea obviously is of neurotic origin, being com- 
monly of a rapid, shallow type like that associated with frank 
cases of hysteria. Sighing respiration also is frequently met with, 
and the respiratory rate is immoderately accelerated — to 70 or 80 
per minute — in acute dyspneic attacks. As a rule, the foregoing 
signs are inconspicuous so long as the subject is at rest, but they 
are immediately provoked by physical stress, excitement, or emo- 
tion, and are peculiar in that their severity is so striking in com- 
parison with the trivial nature of their immediate exciting cause. 
Pallor, excessive perspiration, and peripheral cyanosis are familiar 
objective findings, and occasionally the local syncope and cyanosis 
of true Raynaud's disease are observed. 

Palpation. — Actual displacement of the apex-beat sufficient to 
indicate enlargement of the heart does not occur as a sign of this 
disorder, although many cardiacs of this type have moderate com- 
pensatory hypertrophy due to the physical stress of their occupa- 
tion, and in such the apical impulse is correspondingly forcible. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 407 

The pulse-rate is increased, especially after exercise, even slight 
exertion accelerating the beat to 170 or 180 per minute, and ordi- 
narily the original pre-exercise rate does not return until after the 
lapse of more than the normal two-minute interval. (See p. 403.) 
The inspiratory acceleration and expiratory retardation of sinus 
arhythmia (q. v.) are frequently encountered, and, less commonly, 
the premature contractions of extrasystolic arhythmia (q. v.), the 
latter sort of irregularity tending entirely to disappear after ade- 
quate calisthenic treatment, and being regarded as of no moment 
so long as the heart's functional capacity remains unimpaired and 
its size is not increased. The blood-pressure, both systolic and di- 
astolic, almost constantly is higher than the normal standard, but 
extreme hypertension is not a common rinding. Precordial ten- 
derness, usually circumscribed at or just below the apex, is fre- 
quently elicited, and, rarely, there is spontaneous pain, superficially 
like that of an anginal attack, both of these disturbances being at- 
tributable to the state of existing cardiac overaction and irritation. 

Percussion. — Ordinarily percussion affords nothing very definite, 
inasmuch as any existing enlargement of the precordial area, pecu- 
liar to the individual case, is too trifling to be delimited with any 
degree of accuracy by this method of inquiry. Percussion must 
needs be of little real value in the routine examination of this type 
of cases for the reasons already explained elsewhere. (See p. 361.) 

Auscultation. — Systolic functional murmurs (apical, basic, and 
right sided) are quite commonly audible, but rarely are they at- 
tended by corroborative signs of organic cardiac embarrassment, 
decompensation, and other evidences of structural changes in the 
myocardium. Such sounds, which are most likely to be evanescent 
and readily influenced by exercise and postural changes, should be 
held to be negligible if the subject's response to effort is normal 
and if his heart is not increased in size (Sir James Mackenzie). 
Stethoscopic proof of the existence of one of the varieties of arhyth- 
mia referred to above confirms the palpatory signs of such irregu- 
larities. 

Diagnosis. — The direct recognition of soldier's heart is based upon 
Lewis' "effort syndrome" — tachycardia, palpitation, dyspnea, pre- 
cordial pain, and arterial hypertension unduly exaggerated in 
response to emotion, exercise, and posture. To these cardinal de- 
tails of the clinical picture should be added certain functional ner- 
vous phenomena (exhaustion, insomnia, headache, mental depres- 
sion, and irritability) commonly affecting a man whose sedentary 
habits and lack of exercise during civil life are a striking contrast to 



408 PHYSICAL DIAGNOSIS 

the unaccustomed physical strain and mental shocks to which a 
soldier on active service is subjected. An additional helpful rinding 
is the failure of a heart thus affected to diminish about i cm. (0.39 
inch) in size after active exercise, as the normal heart does. 

Organic disease of the heart is differentiated by the failure to de- 
tect unequivocal signs of decompensation, abnormal extension of 
the cardiac outline, characteristic murmurs and other tonal changes, 
and similar evidences of muscular and valvular defects. Aside 
from these more obvious signs, the past medical history of the sub- 
ject is to be reviewed in instances about which doubt exists, in the 
absence of more significant data. 

ACUTE FIBRINOUS PERICARDITIS (Acute Plastic Pericarditis) 

Clinical Pathology. — In this type of pericarditis the visceral 
and parietal layers of the pericardium are covered, universally or in 
patches, with a fibrinous exudate attended by little or no serous 
effusion, the underlying serosa being dull, swollen, hyperemic, and 
often ecchymotic. In recent cases of mild grade the fibrinous exudate 
is represented by a delicate pliable membrane of yellowish-gray 
color and readily detachable from the underlying serous surface, but 
in older lesions the deposit is thick, tough, and firmly adherent. 
Owing to the movements of the heart, the exudate presents a ridged 
or roughened or shaggy appearance, in some instances matted and 
meshed like two buttered surfaces which have been pressed together 
and then separated, while in other instances innumerable shreds of 
fibrin attached to the pericardium produce the peculiar shagginess 
distinctive of the so-called " hairy heart," known as the cor hirsutum 
or cor villosum. Myocardial inflammation occurs in severe cases 
and may be attended by dilatation, but in mild pericarditis no mus- 
cular changes arise. 

Physical Signs. — Inspection. — This shows nothing characteristic, 
but it is commonly observed that the apex-beat is rapid, heaving, and 
unnaturally diffuse, that the respirations are hurried and irregular, 
and that the patient's face shows anxiety and pain. Diastolic 
pulsation near the second left interspace is a frequent sign in in- 
cipient cases (v. i.). 

Palpation. — With more or less constancy vibrations produced by 
the to-and-fro rub of the roughened pericardial surfaces are felt, 
especially toward the base of the heart. This tactile equivalent of 
the friction sound is usually more intense when the subject is erect 
than when dorsal recumbency is assumed, and can sometimes be 



DISEASES OF THE CARDIOVASCULAR SYSTEM 409 

exaggerated by moderate, and obliterated by forcible, pressure with 
the palm of the hand. Unlike an endocardial thrill, pericardial 
friction fremitus is a very superficial vibration, does not exactly 
coincide with the cardiac beats, and has a peculiar grating quality 
quite unlike the purring vibrations of an eddying blood-stream. 
(See p. 336') 

Percussion. — In so far as it relates to the pericardial inflammation, 
percussion is wholly negative, although in the presence of cardiac 
dilatation, which may develop as a consequence, a corresponding 
extension of the precordial area can be mapped out. 

Auscultation. — The pericardial friction-sound is characteristic of 
pericardial inflammation, if three other potential, though rare, 
factors of such a sound can be excluded: excessive dryness and vis- 
cosity of the pericardium, as in Asiatic cholera, and the existence of 
pericardial eccnymoses and milk-spots. Since the pericardial 
friction-sound has been discussed at length in another place (p. 397), 
it is sufficient here to note, in passing, that ordinarily the sign is most 
distinctly heard at the cardiac base and along the left sternal 
border; that it has a double rhythm not exactly synchronous with 
that of the heart; that it resembles a surface sound, more or less 
influenced by local pressure and by the force of the cardiac impact ; 
and that its quality ranges between that of a soft papery rustle and 
that of rude parchment-like grating or even of creaking leather — 
bruit de cuir neuf. 

Diagnosis. — The friction-sound, precordial pain, and moderate 
fever are the three physical signs pointing to acute plastic pericar- 
ditis. An intense clanging accentuation of the pulmonic second 
sound (Turrettini's eclat clangoreaux diastolique) accompanies, if 
not precedes, the friction-sound in many instances, especially those 
in which the infection is circulatory rather than by extension from a 
pleuritis. The pleuropericardial friction-sound of pleurisy differs 
from a true pericardial rub in being most intense along the left edge 
of the heart, and in having the characteristics of a cardiopulmonary 
sound which is definitely affected by the different respiratory phases 
in the manner elsewhere explained. (See p. 172.) In differen- 
tiating a murmur of endocarditis the punctum maximum, area of 
transmission, pulse peculiarities, cardiac tonal changes, and at- 
tendant myocardial alterations are the dependable criteria. (See 
P- '383O 



4IO PHYSICAL DIAGNOSIS 

SEROFIBRINOUS PERICARDITIS (Serous Pericardial Effusion) 

Clinical Pathology. — In this type an initial stage of dry serositis 
is soon succeeded by the escape of an abundant serofibrinous effusion 
from the engorged capillaries, the serum thus poured out collecting 
within the pericardial sac and the fibrin being deposited upon the 
serous surfaces in the form of a coating of variable thickness and 
distribution. The effusion may be virtually a clear serous fluid, 
but, as a rule, it is more or less opaque from the presence of 
fibrin-flakes and leukocytes, while in conditions of cachexia, in 
tuberculosis, and in malignant disease the liquid is not unlikely to be 
blood stained. The volume of the effusion may range from a few 
ounces to 10 (300 cc.) or more; exceptionally, as in the case of gradu- 
ally accumulating effusions, it amounts to, or even exceeds, a quart 
(1000 cc). Chemically and microscopically, a pericardial exudate 
does not differ materially from inflammatory fluids derived from other 
serous membranes. (See p. 53 .) Complete absorption of an effusion 
containing little or no fibrin may leave the pericardial serosa practically 
unimpaired, but as a rule sufficient plastic material remains after the 
absorption of the serous exudate to cause a variable degree of fibrous 
union between the opposed serous layers. Local deposits of organized 
fibrin are recognized as milk-spots or indurated white opaque areas 
on the visceral pericardium. The myocardium shows degenerative 
or inflammatory changes, and endocarditis commonly coexists, 
usually in consequence of the same factor responsible for the peri- 
carditis, but exceptionally arising by extension of the serosal in- 
flammation through the myocardium. 

Physical Signs. — Inspection. — In the young child a large effusion 
causes unnatural prominence of the precordia, but the more rigid 
chest-wall of the adult does not perceptibly bulge in this manner. 
The apex-beat, if not wholly obscured by the effusion, is visibly 
enfeebled and displaced from its accustomed site. Ordinarily, 
there is pulsation an interspace or two above the normal apical 
area, 1 though sometimes the apex-beat is lowered, owing to depression 
of the diaphragm by a copious, heavy exudate within the pericardial 
sac. In this event there may be also a local epigastric prominence 

1 To all intents and purposes this represents the apex beat, though, as Ewart 
insists, there is good reason, in some instances, to attribute the impulse to the 
impact of the body of the right ventricle. Calvert's recent researches show 
that the position of the heart depends chiefly upon its size, the apex remaining 
in the normal position so long as compensation is preserved and the size of the 
heart is unaltered, but being displaced backward and toward the right when, 
with failing compensation, the heart becomes unduly small by fault of a dimin- 
ished blood-supply. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 41 1 

(Auenbrugger's sign), due to descent of the left lobe of the liver. 
Ewart's sign, or prominence of the sternal end of the left first rib 
with elevation of the head of the clavicle, is a finding of some sugges- 
tiveness. Other associated signs, of variable constancy, include re- 
striction or abolition of the diaphragm shadow, left unilateral diminu- 
tion of expansion, and rapid, difficult breathing, sometimes amounting 
to orthopnea. There may be cyanosis or chalky pallor, engorgement 
of the veins of the neck, and pressure phenomena, such as extreme 
precordial oppression and pain, distressing cough, dysphagia, hoarse- 
ness, and even aphonia. 

The detection by the fluoroscope of the normal inspiratory clear 
zone between the diaphragm and the cardiac apex is proof positive 
of no fluid in the pericardial sac. Little or no transmission of ven- 
tricular pulsation to the air bubble in the stomach is a rontgeno- 
scopic sign upon which Maragliano lays stress in the diagnosis of an 
intervening mass of pericardial fluid. 

Palpation. — The palpating hand confirms the findings noted by 
visual examination, particularly those relating to precordial fulness, 
the apical impulse, the respiratory embarrassment, and the altered 
anatomic relations on the left side. In some instances basal friction 
is palpable, despite the accumulation of considerable fluid in the 
pericardial sac. 

The pulse is usually found to be of increased frequency, low 
tension, and disordered rhythm. Though by no means pathog- 
nomonic, the pulsus paradoxus, which dies out at the end of 
inspiration, is a sign of some corroborative value in the diagnosis 
of a large effusion. (See p. 346.) 

Percussion. — Percussion reveals an unnaturally large area of 
cardiac flatness, which in a bulky effusion may conform to the 
outline of a pyramid having its base downward and its apex in the 
upper sternal region. Diminution in the size and alteration in the 
shape of this area of flatness are occasionally demonstrable when 
the subject changes from an erect posture to dorsal decubitus. The 
normal acuteness of the cardiohepatic angle is made obtuse by the 
sagging of the pericardial sac, and flatness is substituted for the 
resonance normally found in the fifth right interspace at the sternal 
border — Rotch's sign. An effusion of too moderate a size to produce 
well-defined precordial flatness will afford this suggestive area 
of flatness in the space between the borders of the heart and the 
liver. (See Fig. 134.) The upper inner angle of Traube's space 
may be encroached upon by an effusion of large volume. It may 
be possible to delimit an obtuse angle formed at the level of the 



412 PHYSICAL DIAGNOSIS 

third costal cartilage by the normal area of supracardiac vascular 
dulness and the left border of pericardial flatness — Sibson's notch. 
Compression of the lower lobe of the left lung by an effusion of 
large volume may produce, in the left infrascapular region, a small 
patch of dulness over which increased vocal fremitus, bronchophony, 
and bronchial breathing are detected when the patient sits erect, but 
not when he leans forward, lies in right lateral decubitus, or assumes 
the knee-chest posture (Bamberger; Pin); or there may be dulness, 
with abolished voice and respiratory sounds, at the base of the left 
lung alongside the spine (Ewart). In certain instances a circum- 
scribed patch of bronchial breathing is audible in the right mammary 
region below the nipple. Compression of the left lung by a large 
effusion may account for a midaxillary area of dulness or of skodaic 
resonance, over which the voice and breath-sounds are either sup- 
pressed or greatly exaggerated, and this group of signs also is de- 
cidedly affected by postural changes. 

Auscultation. — The cardiac sounds are indistinct, muffled, or 
inaudible, except at the base, where increased intensity of the second 
sound is the rule. Here also friction-sounds are prone to persist, 
in contrast to the auscultatory silence over the precordia below this 
level. With absorption of the exudate, however, a corresponding 
increase in the extent of the friction area is to be expected, with 
reappearance of the cardiac-sounds. The various modifications of 
the respiratory sounds audible over patches of compression atelectasis 
have been mentioned in the preceding paragraph. 

Diagnosis. — Displacement and enfeeblement' of the apex-beat, 
an enlarged precordial area of pyramidal outline, flatness in the 
cardiohepatic angle, muffling of the heart-sounds, and evidences of 
pulmonary compression are the principal diagnostic signs of an 
effusion in the pericardial sac. 

In differentiating cardiac dilatation it is helpful to remember that 
the apex-beat of a dilated heart marks the extreme lower and outer 
limit of the cardiac outline, and does not lie well within this boundary, 
as it does in a pericardial effusion; and that the flatness of a dilated 
heart, though exceptionally pyramidal, is generally of ovoid shape, 
does not extend so high as the flatness 'of an effusion, and shades off 
gradually into the surrounding pulmonary resonance, so that no 
sharp line of demarcation between the two is appreciable, as is 
usually the case with effusion flatness. A history of chronic valvular 
disease or of myocarditis suggests dilatation, just as a story of rheu- 
matic fever and acute plastic pericarditis is in favor of effusion. 
Neither the character of the apical impulse nor the effect of postural 



DISEASES OF THE CARDIOVASCULAR SYSTEM 413 

changes on the area of cardiac flatness is a reliable differential point; 
and the cardiohepatic angle may be dulled by a dilated right ventricle. 

A left pleural effusion, especially when encapsulated near the 
heart, may suggest a pericardial effusion of large volume, but ordi- 
narily a confusion of this sort is disposed of without difficulty. Pleu- 
risy is indicated by the history of an acute stitch in the side, a pleural 
friction-sound, Grocco's sign, flatness over the anterolateral and 
generally the posterior regions of the thorax, and by the failure to 
discover such important pericardii signs as basal friction, extension 
of precordial flatness, and enfeeblement of the cardiac tones. In 
the event of a puzzling group of physical signs, as in the case of 
coexisting pericardial and pleural effusion, the x-ray may settle the 
diagnosis beyond all question. 

Exceptionally, enlargement of the area of cardiac flatness is 
referable to pulmonary retraction, to aortic aneurism, or to mediastinal 
neoplasm, but none of these conditions creates pyramid-shaped 
flatness, and each of them is attended by physical signs and by a 
clinical history that, if intelligently reviewed, are sufficient for 
differentiation. 

PURULENT PERICARDITIS (Pyopericardiam ; Empyema of the Pericardium ; 
Pericardial Abscess) 

Clinical Pathology. — This most grave variety of pericarditis, 
characterized by an effusion of pus within the pericardial sac, is more 
frequent in children than in adults, and generally is traceable to 
pyemia, to some neighboring local purulent focus, or to an acute 
specific infectious process like pneumonia or tuberculosis. The 
exudate varies in character according to conditions prevailing in the 
individual case, being in some a thin limpid liquid and in others a 
collection of creamy material containing a minimal amount of serum 
and fibrin and composed chiefly of pus cells, the extraordinary number 
of which constitutes the striking difference between this and the 
ordinary serofibrinous type of effusion. The pus is but rarely 
absorbed spontaneously, although sometimes the more liquid portions 
are thus disposed of, leaving an amorphous mass of caseous matter 
tending ultimately to undergo calcification. Instrumental evacuation 
of the pus results in permanent adhesion of a variable area of the 
two pericardial layers, already unduly thickened and granular from 
the intense purulent inflammation by which they have been attacked. 
Spontaneous evacuation of a pericardial abscess, as, for example, 
by its discharge through the chest wall or into the mediastinal cavity, 
is a possible, but very remote, sequel, should the patient live. It i= 



414 PHYSICAL DIAGNOSIS 

obvious that the myocardial changes in purulent pericardial effusions 
must be of greater intensity than those attending simple serofibrinous 
exudates, and in some instances purulent infiltration of the heart 
muscle takes place. 

Physical Signs. — The aspirating needle is the only certain means 
of distinguishing a purulent from a serofibrinous pericardial effusion 
whose local subjective signs are practically identical. On academic 
grounds it is sometimes taught that extreme precordial bulging and 
hepatic displacement, with local edema or even discoloration, mean 
pus in the pericardial sac, but, clinically, this dramatic symptom- 
group virtually never appears. It is not unusual, however, to find 
great prostration, rapid emaciation, recurrent rigors, widely fluctua- 
ting fever, leukocytosis, and iodophilia in purulent cases, together 
with a history of some cause capable of setting up a purulent inflamma- 
tion. But inasmuch as the foregoing evidence is more often equivocal 
than definite, pericardicentesis, in the vast majority of cases, is the 
key to the situation. (See p. 55.) 

CHRONIC ADHESIVE PERICARDITIS (Adherent Pericardium; Mediastino- 

pericarditis) 

Clinical Pathology. — Pericardial adhesions, formed by the 
organization of inflammatory material, ordinarily are the relic of a 
well-defined attack of acute pericarditis, but in some instances the 
fibrosis arises insidiously, with no authentic history of a primary 
inflammation. In either event the process is essentially of a chronic 
nature, and, in accordance with its anatomic distribution, is separable 
into two principal groups, the internal and the external, which types, 
it is to be remembered, are frequently combined. Internal pericardial- 
adhesions, confined to the pericardial sac, commonly exist as scattered 
fibrous strands or filaments connecting the parietal and visceral 
layers of the pericardium, which also is generally the seat of con- 
siderable thickening and induration. These strands vary in length 
according to their situation, being longest near the apex of the heart, 
where the cardiac excursions exert the greatest traction, and, as the 
result of this strain, a filament may be torn from one of its attachments, 
so that it dangles free in the pericardial cavity. In some cases the 
adhesions are represented merely by a few patches of simple union 
between the two membranes, and in others a moderate fibrosis of 
the pericardium, rather than actual adhesions, is the predominant 
lesion, conditions such as these often being quite symptomless and 
leading to no damage to the myocardium. In contrast to these 
relatively benign local processes, it occasionally happens that the 



DISEASES OF THE CARDIOVASCULAR SYSTEM 415 

parietal and visceral pericardium are universally adherent, thickened, 
and tightly welded into a single structure, the normal pericardial sac 
being, in consequence, entirely obliterated, and to this condition 
the term adherent pericardium is applicable. Investment of the 
heart by an unyielding bony capsule supervenes when an adherent 
pericardium undergoes calcification, as is the case in exceptional 
examples of this type of fibrosis. In early life the incessant com- 
pression exerted by a dense and firmly contracting adherent peri- 
cardium is capable of causing actual atrophy of the heart. External 
pericardial adhesions, almost always attended by internal union of 
the layers, may anchor the outer surface of the pericardium to the 
adjacent chest- wall, the pleura, the diaphragm, and the mediastinal 
structures — a most serious condition of indurative mediastinoperi- 
carditis (q. v.), tending to cause great hypertrophy and dilatation 
of the heart, advanced myocardial degeneration, and sometimes 
to provoke inflammatory implication of the subphrenic structures. 
The cardiac enlargement commonly but by no means invariably 
met with in the different types of chronic adhesive pericarditis, 
especially when external adhesions exist, is attributable to several 
factors : hypertrophy and subsequent dilatation may be due to mechan- 
; cal interference with the movements of the heart, to compression 
stenosis of large arterial trunks, or to associated valvular defects, 
while pure dilatation is frequently set up by the coexisting myo- 
carditis. The right ventricle, being relatively weak, thin-walled, 
and predisposed anatomically to external adhesions, is likely to be 
damaged more seriously by these structural changes than the left 
ventricle. 

Physical Signs. — Inspection. — Visual examination may discover 
practically all the important evidences of chronic adhesive peri- 
carditis, or those referable to fixation of the heart to neighboring 
structures and to the direct tug upon different parts of the chest-wall 
produced by the contractions of the adherent organ. There may 
be no physical signs whatever of adherent pericardium, in the absence 
of adhesions between the external layer of the sac and the thoracic 
wall, diaphragm, and pleura. In the presence of extensive adhesions 
there is fixation of the apex-beat, which being restricted and bound 
down by fibrous tissue, cannot gravitate toward the dependent side 
when the subject changes from left to right lateral decubitus or vice 
versa, nor can it descend at the close of a full inspiration. Systolic 
retraction of a small area of the thoracic surface in the neighborhood 
of the apex is also noted; rarely a similar recession of several inter- 
spaces and their corresponding costal cartilages to the left of the 



416 PHYSICAL DIAGNOSIS 

sternum, and even retraction of the lower part of this bone are 
perceived. Sometimes there is a decidedly undulatory precordial 
impulse — Sander's sign. J. F. H. Broadbent has described, as a 
pathognomonic sign of extensive pericardial adhesions, systolic 
retraction of the tenth and eleventh intercostal spaces in the left 
infrascapular region, and also, less commonly, of the seventh and 
eighth interspaces anteriorly — Broadbent' s sign. (See p. 332.) 
Under the same circumstance Sir William H. Broadbent has noted 
that the normal epigastric movements during respiration are greatly 
hampered, if not quite abolished. Friedreich's sign (diastolic collapse 
of the jugular veins) and Kuss maid's sign (inspiratory jugular tumes- 
cence) are inconstant findings, in no wise distinctive of adhesive 
pericarditis. (See p. 334.) As the right ventricle fails, dyspnea 
becomes distressing, cyanosis appears, and edema and other forms 
of dropsy develop. Anasarca and effusions into the peritoneum 
and the pleura have been observed as the effect of pressure upon 
the large azygos vein (J. Lloyd Roberts). 

Palpation. — Exceptionally, a diastolic shock is felt over areas that 
show systolic retraction, and this sign, due to the sudden rebound of 
the chest-wall directly after systole, is regarded as diagnostic. 
As in pericardial effusion, the pulse in adhesive pericarditis not 
uncommonly conforms to the paradoxic type. The fixed position 
of the apex-beat is clearly appreciated by palpation. 

Percussion. — The area of cardiac flatness may be increased, 
commonly in all directions, the increase being referable both to the 
enlargement of the heart and to fibrosis and retraction of the anterior 
margins of the lung. If the latter be anchored by pleuropericardial 
adhesions, comparative percussion will fail to show the diminution 
of cardiac flatness which occurs normally at the end of a full inspira- 
tion. Dulness in the cardiohepatic angle has been found in adhesive 
pericarditis, as well as in pericardial effusion (q. v. s.). 

Auscultation. — There are no definite auscultatory evidences of 
true adherent pericardium, but in mediastinopericarditis there may 
be a peculiar creaking friction-sound audible over the sternum dur- 
ing up-and-down movements of the subject's arms (Perez; Bab- 
cock). (See p. 172.) A pericarditic friction-sound, not unlike the 
presystolic rumble of mitral stenosis (q. v.), is present in some cases, 
but not with any degree of constancy. In the presence of exten- 
sive adhesions pleuropericardial friction-sounds are commonly 
heard over the anterior pulmonary borders surrounding the body 
of the heart. The cardiac sounds are those of hypertrophy or of 
dilatation, according to which condition predominates. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 417 

Diagnosis. — Fixation of the apex-beat, immobility of the anterior 
pulmonary borders, systolic retraction and diastolic shock, cardiac 
enlargement, pericarditic friction, paradoxic pulse changes, and 
phenomena relating to the jugular veins form a combination of signs 
that unmistakably indicates chronic pericarditis with extrapericar- 
dial adhesions, and in such cases a history of previous pericarditis is 
usually obtainable, to make the diagnosis doubly certain. As 
noted above, simple internal adhesion of the two pericardial layers 
is essentially a latent process, giving rise to no distinctive symptoms 
nor physical signs. In doubtful cases — and these are numerous — 
one can venture only a provisional diagnosis, based upon a history 
of pericardial inflammation, and upon a clinical picture of chronic 
circulatory failure, respiratory distress, right ventricular dilatation, 
and, sometimes, friction-sounds over the precordia. 

Pericarditic hepatic pseudo cirrhosis, associated with ascites and 
with a hard, contracted liver, counterfeits ordinary alcoholic cirrho- 
sis of this organ, especially in those cases in which the cardiac phe- 
nomena are latent or overshadowed by those of portal obstruction. 
In this differentiation, apart from the cardiac signs, Laennec's 
cirrhosis is suggested by a history of alcoholism or of syphilis, by a 
symptomatology characterized by long-standing gastro-intestinal 
catarrh, hematemesis, melena, and hemorrhoids, and by the appear- 
ance of ascites followed by edema of other parts. In contrast, Pick's 
pseudocirrhosis is indicated by a history of rheumatism, by symptoms 
referred to the heart, and by the onset of edema of dependent parts 
prior to the development of ascites. 

HYDROPERICARDIUM (Pericardial Dropsy) 

Hydropericardium is usually part of general dropsy, cardiac or 
renal, but it may arise in consequence of the pressure of an aneurism 
or of a mediastinal neoplasm. Under exceptional circumstances 
the fluid, instead of being a clear serum, is milky from the presence 
of chyle — chylopericardium. The transudate seldom attracts atten- 
tion, for, being non-inflammatory and of moderate volume, it does 
not readily to provoke conspicuous objective symptoms. Physical 
signs, when present, include moderate dyspnea and perhaps pre- 
cordial uneasiness, with the flatness of a liquid pericardial effusion 
which most readily shifts with changes of posture, and which is 
unaccompanied by friction, fever, pain, or precordial prominence. 
These peculiarities plus a story of cardiorenal disease and the dis- 
covery of subcutaneous dropsy or of hydrothorax, serve to differen- 
tiate hydropericardium from a pericarditic effusion. 



41 8 PHYSICAL DIAGNOSIS 

HEMOPERICARDIUM (Pericardial Hemorrhage) 

Hemopericardium, or free hemorrhage into the pericardial sac, 
is a rare and rapidly fatal accident, and one to be clearly distin- 
guished from the hemorrhagic pericarditic effusions sometimes 
met with in tuberculous, cancerous, and cachectic subjects (see p. 410) . 
Ordinarily hemopericardium is due to the bursting of aneurism 
springing from the intrapericardial portion of the aorta or from a 
coronary artery; exceptionally the blood pours out from a chamber 
of the heart ruptured by fault of advanced myocardial destruction; 
and sometimes the hemorrhage follows a wound of the heart. In 
any event the physical signs are those of effusion, and are attended 
(as well as overshadowed) by acute dyspnea, precordial pain, 
shock, and circulatory failure. 

PNEUMOPERICARDIUM (Pyopneumopericarditim; Hydropneumo- 
pericarditim ; Hemopneumopericardium ) 

Pneumopericardium, or the presence of gas within the pericardial 
sac, is almost invariably associated with a liquid effusion, usually 
purulent (pyopneumopericardium) , sometimes serous (hydropneu- 
mopericardium) , and exceptionally hemorrhagic (hemopneumo- 
pericardium) . The affection usually depends upon the entrance 
of air through a traumatic breach or by way of a fistulous tract 
leading from a neighboring organ, but the pericardium may fill with 
gas generated by the decomposition of an exudate therein. Owing 
to the practical constancy of bacterial contamination, purulent 
pericarditis is a very frequent complication. The direct effect of 
pneumopericardium is distention of the pericardial cavity with gas 
and with liquid, the former occupying the upper, and the latter 
filling the lower, part of the space. This distention, if decided, leads 
to embarrassment of the cardiac action and to displacements of 
the heart, lungs, and diaphragm similar to those met with in ordi- 
nary liquid pericardial effusions. 

The physical signs vary with the degree of pericardial distention 
and with the character and the volume of the exudate. The pre- 
cordial interspaces are leveled or bulged and the precordia itself 
may be unnaturally prominent; the apex-beat is obscure, if not 
wholly effaced, but it may become both visible and palpable when 
the subject leans forward so as to bring the heart closer to the parietes. 
There is tympany (perhaps with a metallic or a cracked-pot tone) 
over the upper part of the cardiac area, with flatness below, as the 
liquid effusion accumulates, the relative positions of these two areas 






DISEASES OF THE CARDIOVASCULAR SYSTEM 419 

being modified by postural changes. Auscultation, which affords 
most distinctive signs, reveals more or less pericardial friction inter- 
mingled with a medley of churning, splashing, tinkling sounds, 
among which can be distinguished the hard tone of the metallic 
gurgle and the liquid purl of the bruit de moulin (see p. 400) . These 
adventitious sounds, synchronous with the movements of the heart, 
may effectually mask the cardiac tones, and the rising pericardial 
exudate has a similar effect. Extreme pneumopericardial distention 
is likely to cause great dyspnea, cyanosis, severe precordial oppres- 
sion and pain, distressing palpitation, syncopal attacks, and a small, 
erratic pulse; but in less urgent cases the picture is very like that of 
pericarditis. 

Pneumopericardium must be distinguished from left pneumo- 
thorax and from gaseous distention of the stomach, the differentiating 
points in the first instance being a displaced and pulsating cardiac 
area associated with metallic and splashing sounds of palpably 
respiratory origin, and in the second instance the disappearance of 
similar adventitious sounds immediately after the passage of a 
stomach-tube to remove the gas. 



cardiac hypertrophy 

Clinical Pathology. — An adequately nourished heart subjected 
to habitually increased work in time undergoes hypertrophy, or an 
increase in its muscular structure, this enlargement being designated 
as general or as partial, according to its distribution. Not infre- 
quently a single chamber is affected, or the change may be restricted 
to one entire side or to a chamber on each side, while a still sharper 
limitation of the hypertrophy to a small local area of the heart is 
termed circumscribed. Pathologically, two well-defined types of 
cardiac hypertrophy are recognized: simple hypertrophy, or thickening 
of the cardiac wall with no deviation from normal in the size of the 
corresponding chamber; and, eccentric hypertrophy, in reality hyper- 
trophy with dilatation, characterized by thickening of the wall with 
enlargement of the chamber. So-called " concentric hypertrophy," 
or thickening of the wall with diminution in the size of the cavity, 
is a fictitious condition, created no doubt by arrest of the heart's 
action during systole or by postmortem ventricular contraction. 

The weight, size, and shape of a hypertrophied heart deviate 
from the normal according to the degree and site of the enlargement. 
In examples of moderate hypertrophy the normal average weight is 
commonly doubled, and in extreme instances is exceeded four- or five- 



420 



PHYSICAL DIAGNOSIS 



fold, as in the enormous "ox-heart" hypertrophy, or cor bovinum 
(Fig. 165). Corresponding increase in the thickness of the cardiac 
walls develops, even in eccentric hypertrophies, despite the apparent 
parietal thinning referable to the coexisting dilatation. The papillary 
muscles and the muscular columns within the ventricles are thick- 
ened and diminished in resiliency. When there is predominant hy- 
pertrophy of the left ventricle, the heart becomes elongated and the 
apex unduly blunt and displaced downward and to the left; when 
the right ventricle is enlarged, the contour of the heart becomes 
more spherical than normal, the breadth being conspicuously 




Fig. 



Normal 
164.- 



Comparative sizes 'of the ventricles in a normal and a hypertrophied 
heart (Philadelphia General Hospital). 



increased and the lengthening less apparent; hypertrophy of botl 
ventricles causes commensurate elongation of the organ, with unnat- 
ural flatness, breadth, and bluntness of the apex; and in hypertrophy 
of the entire heart both the length and the breadth are exaggerated, 
generally with approximate preservation of the normal contour. 
Pure hypertrophy deepens the color and increases the consistence 
and resistance of the cardiac muscle, but when fibrous and fatt] 
changes coexist, as is usually the case, the deep-red color of the 
hypertrophy becomes correspondingly paler, and the muscle under- 
goes more or less fibrous induration and fatty softening. The his- 
tologic changes in hypertrophy consist of an increase in the size of 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



421 



the individual muscle-fibers, and, in all probability, of an increase in 
their number. 

Left-sided and ventricular hypertrophies are more common than 
right sided and auricular, the four chambers of the heart being 
affected in the following order of frequency: left ventricle, right 
ventricle, right auricle, and left auricle. The causes of cardiac 
hypertrophy consist of arteriosclerosis, valvular and parietal affec- 
tions of the heart, and persistent cardiac overaction due to various 
irritating influences. 

General hypertrophy occurs in advanced age as the result of the 
increased peripheral resistance incident to senile arteriocapillary 




Fig. 164a. — Radiograph of cardiac hypertrophy and dilatation. 

Manges.) 



(Plate by Dr. W. F. 



changes; it frequently attends myocardial fibrosis and adherent 
pericardium, which mechanically hamper the heart's movements; 
and it develops in conditions provocative of excessive cardiac fre- 
quency and force — i. e., the tachycardia and palpitation excited by 
hyperthyroidism ("kropfherz"), by the neurosis termed paroxysmal 
tachycardia, and by nicotin, caffein, and sexual excesses. Alcohol 



42 2 PHYSICAL DIAGNOSIS 

is an active cause of cardiac hypertrophy, since it not only stimulates 
the cardiac action and induces arteriosclerosis, but also, in the case 
of those who consume large quantities of malt liquors, adds to the 
heart's nutrition and increases its work by producing hydremic 
plethora. Prolonged physical exertion eventually leads to general 
hypertrophy, but especially to enlargement of the left ventricle. 
Primary congenital cardiac hypertrophy is, according to Virchow, in 
reality a diffuse myomatous neoplasia. 

Left ventricular hypertrophy accompanies aortic stenosis, aortic 
regurgitation, and mitral regurgitation, for in the first lesion the 
ventricle labors hard to empty its contents, and in the other two it 
must propel an excessive volume of blood. Stenosis of the aorta 
and, less commonly, aortic aneurism, when they impede the main 
arterial current, are factors of left ventricular hypertrophy. Arte- 
rial hypertension in combination with mitral stenosis produces an 
extreme grade of left ventricular hypertrophy, even greater than 
that ordinarily met with in arterial sclerosis plus aortic lesions or 
chronic nephritis (Thomas Lewis). In states of arterial hyper- 
tension and general arterial sclerosis the left ventricle hypertrophies 
to overcome increased peripheral resistance. 

Right ventricular hypertrophy is usually traceable to obstruction of 
the pulmonary circulation resulting either from mitral defects or 
from pulmonary cirrhosis, emphysema, inflammatory thickening 
of the pulmonary arterioles, or widespread pleural adhesions; 
less commonly, obstruction of the pulmonary orifice is the cause 
of the enlargement. 

Auricular hypertrophy is invariably attended by dilatation; if left- 
sided, hypertrophy of the auricle means mitral disease, especially 
stenosis ; while hypertrophy of the right auricle is generally due to 
intrapulmonary hypertension and its consequences, or, exceptionally, 
to organic tricuspid lesions. 

Physical Signs. — Left Ventricular Hypertrophy. — On inspection 
the precordia may appear more prominent than normal if the subject 
be a child (Fig. 40, p. 91). and the apex-beat, which is violent and 
unnaturally extensive, is visibly displaced toward the left and down- 
ward. The precordial impulse is tumultuous, the arteries throb 
excessively, and in the extreme case the patient's body jogs rhythm- 
ically with every beat of the heart. Palpation demonstrates the 
powerful action of the enlarged heart, whose impact is appreciated 
as a deliberate, heaving thrust which counteracts the pressure of the 
examiner's palm and distinctly lifts it with systole. The pulse 
indicates high arterial tension, and is full, regular, well sustained, 



DISEASES OF THE CARDIOVASCULAR SYSTEM 423 

and of normal or somewhat diminished rate. Percussion reveals 
extension of the cardiac area, vertically upward, horizontally outward, 
and obliquely downward, the upper limit sometimes reaching to the 
second interspace, the left border extending well beyond the left 
midclavicular line, and the lower margin being at the level of the 
sixth or seventh interspace. Auscultation elicits a loud and prolonged 
mitral first sound at the apex, the tone in this situation being di>- 
tinguished by the dull booming quality of its dominant muscular 
component. The aortic second sound is greatly accentuated, being 
loud and clear and ringing. In the event of unequal intraventricular 
tension (and this is common) , the second sound is reduplicated, and 
in some instances there is also doubling of the first sound. In pure 
hypertrophy, to which the foregoing signs apply, murmurs are not 
audible. 

Right Ventricular Hypertrophy. — Inspection discovers systolic 
pulsation in the epigastrium, at the left sternal border between the 
fifth and seventh costal cartilages, and sometimes at the right sternal 
border between the third and fifth cartilages. In extreme hypertrop hy 
the lower sternal region and the apex of the epigastrium appear 
abnormally prominent. The apex-be? t is diffuse, and displaced 
horizontally toward the left, with little or no depression. Palpation 
of the epigastrium commonly detects a heaving impulse just below 
the subcostal angle, most extraordinarily vigorous thrusts of the 
ventricle being here perceptible in the emaciated subject. The 
transmitted cardiac impulse occasionally palpable over the fiver 
must be distinguished from true hepatic venous pulsation (q. v.). 
The arterial pulse, aside from its somewhat diminished volume, 
presents no noticeable deviation from normal. On percussion the 
precordial limits are found to be expanded chiefly in a horizontal 
direction beyond the right sternal border, dulling the normal pul- 
monary resonance of the cardiohepatic angle and extending 1 inch 
(2.5 cm.) or so to the right of this landmark. Auscultation at the 
tricuspid area shows an intense, prolonged first sound, and at the 
pulmonic area a sharp, intense, sometimes reduplicated second 
sound. Murmurs do not arise, of course, so long as the valvular 
mechanism of the right ventricle remains unimpaired. 

Auricular Hypertrophy. — This is invariably attended by dilatation 
of these chambers, and is recognized chiefly, if not entirely, by the 
discovery of some lesion of the auriculoventricular orifices capable 
of provoking undue intra-auricular pressure. Left auricular enlarge- 
ment cannot be diagnosed by objective symptoms, but the demon- 
stration of mitral disease (especially stenosis) is presumptive evidence 



424 PHYSICAL DIAGNOSIS 

in its favor. The left auricle, in exceptional instances, undergoes 
sufficient hypertrophy to damp the pulmonary vibrations, and 
therefore to impair percussion resonance at the left of the cardiac 
base, but it cannot possibly impinge upon the anterior chest-wall 
to produce visible or palpable pulsations thereupon, as is sometimes 
carelessly taught. {Cf. Mitral Stenosis, p. 454.) Right auricular 
enlargement is easier to distinguish, since well-marked examples are 
accompanied by presystolic pulsation near the sternal ends of the 
third and fourth right interspaces, by encroachment of cardiac 
dulness upon this territory, and by a forcible jugular pulse. The 
character of this venous pulsation is accurately fixed by the sphygmo- 
gram, which indicates an exaggerated wave of either auricular or of 
ventricular origin, as the case may be. (See Figs. 132 and 133.) The 
ability to auscultate the presystolic tone of a contracting hyper- 
trophied auricle, right or left, is a gift possessed by few clinicians. 
Enlargement of the right ventricle and the signs of tricuspid leakage 
or obstruction, particularly the former, complete the clinical picture 
sketched by the signs just noted. 

Diagnosis. — Pure cardiac hypertrophy is betrayed by a most 
distinctive group of signs: a full, regular, high-tension pulse, a 
deliberate heaving precordial impulse, displacement of the apex-beat, 
extension of the cardiac area, and a prolonged, muscular mitral or 
tricuspid first sound with ringing accentuation of the aortic or 
pulmonic second sound. The chamber or chambers chiefly affected 
by the myocardial overgrowth can be identified by reviewing more 
in detail the objective symptoms above enumerated. This can be 
done more accurately by ordinary physical examination than by 
the electrocardiograph, which gives questionable tracings in many 
instances. It is, however, the rule to find in left ventricular hy- 
pertrophy inversion of the it- wave in leads II and III, and in 
right ventricular hypertrophy either a normal or an inverted 
i?-wave in lead I and an enlarged it-wave in leads II and III. 

Simple cardiac overaction may counterfeit hypertrophy, in so 
far as it gives rise to a bounding pulse, strong pulsation of the pre- 
cordia and epigastrium, and intense heart sounds. Here, however, 
the similarity ends, since an excited heart does not alter the position 
of the apex-beat nor enlarge the cardiac area, and, furthermore, as 
soon as the heart quiets down the confusing signs disappear. Bathy- 
cardia, or an unnaturally low position of the heart, may be the 
cause of perceptible epigastric pulsation of excessive force. 

The question of hypertrophy versus cardiac displacement must be 
settled, when the apex beats away from its natural situation, but 



DISEASES OF THE CARDIOVASCULAR SYSTEM 425 

if mere dislocation exists, the cardiac area, despite its abnormal 
situation, remains of normal size and shape. In dealing with a car- 
diac displacement, moreover, it is usually possible to discover the 
lesion that has either pushed or dragged the organ from its accustomed 
position. (See p. 326.) 

Pulmonary cirrhosis, whereby the anterior margins of the lungs 
may be retracted so as to expose the parietal surface of the heart, 
is sometimes attended by vigorous precordial pulsation, by increase 
in the area of cardiac flatness, and by exaggeration of the cardiac 
sounds. In favor of this condition, rather than of true hypertrophy, 
are the absence of a typical booming first sound and of a ringing 
second sound, the failure to detect tumultuous action of the arteries, 
the inability to discover a satisfactory factor of hypertrophy, and 
the presence of definite pulmonary signs. If displaced, the heart 
tends to ride upward and toward the left, as the result of traction 
from these directions. In this connection it is well to recall the fact 
that cirrhosis of the lungs in time induces right ventricular hyper- 
trophy and, ultimately, distention of this chamber. In the presence 
of extensive pulmonary emphysema it is sometimes impossible to 
elicit the physical signs of an enlarged heart, owing to the mass of 
dilated vesicular tissue which separates the heart from the chest-wall. 
Apparent enlargement of the heart, due to extension of its surface 
limits, may depend upon paracardial lesions, such as consolidation 
of the anterior pulmonary borders, circumscribed pleural effusion, 
mediastinal tumor, and aneurism of the aortic arch, though under 
such circumstances careful analysis of the subject's history and 
physical signs suffices for an accurate differentiation. The same 
is true of certain thoracic deformities that may cause undue promi- 
nence of the precordial region. 

The discrimination between pericardial effusion and a heart enlarged 
by dilated hypertrophy has- been discussed under the former affection. 
(See p. 412.) 

CARDIAC DILATATION 

Clinical Pathology. — Dilatation of the heart, or an abnormal 
enlargement of one or more of its chambers, is due to stretching of 
its wall under the stress of overwork in excess of the organ's nutrition 
and muscular power. Intracardiac hypertension and diminished 
parietal resistance, singly or combined, are the essential factors 
which force the cardiac muscle to give way in this manner, either 
suddenly in consequence of an acute strain, or gradually after a 
prolonged period of overwork. In the great majority of instances 



426 PHYSICAL DIAGNOSIS 

the resistance of the myocardium is weakened by structural changes 
such as parenchymatous degeneration and interstitial fibrosis, but 
in others simple exhaustion of the cardiac muscle appears to be the 
sole predisposing cause of the dilatation. 

Dilatation may exist alone or in combination with hypertrophy, 
and, like the latter, may be either a general or a partial change. 
Dilatation with thinning consists of an enlargement of the chamber 
with thinning of its wall, generally of acute development, and pri- 
marily excited by a sudden rise of pressure within the heart. 
Thus, acute distention, particularly of the right heart, some- 
times results from the sudden increase of blood-pressure incident 
to inordinate muscular strain; the myocardium may suddenly yield 
and the corresponding chamber dilate under the intracardiac hyper- 
tension and overdistention due to traumatic valvular insufficiency; 
and acute dilatation may occur whenever the resistance of the 
myocardium is lessened by nutritive defects, and by the action of 
bacterial toxins. 

Dilatation with hypertrophy denotes enlargement of the chamber 
with increase in the cardiac musculature, the wall being either of 
normal or of increased thickness. This type of dilatation, save when 
a degenerated hypertrophied heart suddenly gives way under acute 
strain, is essentially a chronic condition, and intimately associated 
with hypertrophy, of which it usually represents the secondary phase. 
Pure hypertrophy of the heart has certain limitations, fixed by nutri- 
tion, beyond which the overgrowth must cease and undergo retro- 
grade changes, for want of adequate blood-supply through the 
coronary arteries, either because these vessels are atheromatous or 
because of the rapid and disproportionate increase in the volume 
of the cardiac muscle. When this limit is reached, the cardiac 
wall yields to increased pressure from within, so that to the primary 
hypertrophy dilatation is now added. When finally dilatation can 
go no further, for to this change also there must be a limit, the chamber 
surrounded by the weakened muscle fails to empty itself with systole, 
is in consequence still more distended by residual blood, and becomes 
the starting-point of a stasis affecting that part of the circulatory 
system behind the dilated chamber. This means failure of compensa- 
tion, the immediate effects of which are relative mitral leakage, left 
auricular dilatation, and engorgement of the lungs when the left 
ventricle fails, and tricuspid insufficiency, sooner or later followed 
by right auricular dilatation and general venous stasis, when the 
right ventricle yields. These accidents and the consequences 
thereto are considered in connection with lesions of the cardiac 






DISEASES OF THE CARDIOVASCULAR SYSTEM 427 

valves. (See p. 439.) In favorable cases primary dilatation 
of a cardiac chamber is followed by hypertrophy of its wall, in 
order thus to compensate for the impairment of cardiac strength, 
the duration, extent, and efficiency of this increased muscular 
power depending upon the circumstances prevailing in the individual 
instance. So long as the hypertrophy predominates sufficiently 
to ensure complete systolic discharge of the ventricular contents, 
stasis is warded off and the circulation does not suffer, but so soon as 
myocardial degeneration and intracardiac hypertension, one or both, 
become the prevailing change, secondary dilatation, leading to 
permanent circulatory embarrassment, inevitably supervenes. 

Physical Signs. — Left Ventricular Dilatation. — Inspection shows 
enfeeblement of the apex-beat, which is displaced downward and to 
the left of its normal site. The impulse is either diffuse, forceless, 




Fig. 165. — Synchronous sphygmographic tracings of the carotid artery and the apex- 
beat in a case of cardiac dilatation. (Tracing by Dr. G. Bachmann.) 

and undulatory, or, in advanced dilatation, quite imperceptible to 
the eye. On palpation the apical impulse, if at all palpable, can 
be but vaguely felt as a somewhat abrupt tapping or slapping beat, 
utterly unsustained and lacking in strength. It is a common experi- 
ence to encounter a visible apex-beat which cannot be palpated. 
The pulse is rapid, arhythmic, and of diminished volume and tension, 
the individual waves being diminutive and easily extinguished by 
moderate pressure on the vessel (Fig. 165). Percussion defines an 
enlarged cardiac outline whose upper, lateral, and lower limits 
virtually correspond to those of left ventricular hypertrophy (q. v.). 
On auscultation the heart sounds are found to be feeble, impure, 
arhythmic, and perhaps modified by coexistent murmurs. The 
first sound at the apex is short, sharp, and high pitched, having losl 



428 PHYSICAL DIAGNOSIS 

most of its muscular tone, and acquired a valvular quality like that 
of the second sound. In the event of serious ventricular failure 
these two sounds, so accoustically alike, may be approximated by 
an abbreviated diastolic period, so as to reproduce the fetal cardiac 
rhythm termed embryocardia, while in some instances the irregularity 
conforms to the triple beat of gallop rhythm. (See pp. 370 and 379.) 
The tricuspid first sound shows no noteworthy deviation trom 
normal. At the base of the heart the aortic second sound is weakened 
commensurately with the gravity of the left ventricular enfeeblement, 
while the pulmonic second sound, so long as the right ventricle is 
unimpaired, is relatively accentuated. Endocardial murmurs, 
when present, generally indicate relative mitral leakage, though 
preexisting valvular disease should always be credited as a possible 
factor of the bruits. 

Right Ventricular Dilatation. — On inspection and palpation one 
may note suppression of the normal apex-beat and undulatory 
pulsation corresponding to the parietal impact of the enlarged 
flaccid ventricle: below and on either side of the ensiform; outside 
the right sternal border between the fourth and seventh costal car- 
tilages; and close to the left sternal margin between the second and 
fifth cartilages (Fig. 125, p. 329). The arterial pulse is affected by 
attendant conditions more than by the ventricular dilatation, being 
usually of increased frequency, small volume, disturbed rhythm, 
and low tension; the venous pulse, in the face of free tricuspid leakage, 
produces a sphygmogram having a high, blunt ^-wave of the systolic 
or ventricular type. (See Fig. 133, p. 357.) Percussion defines the 
right border of the heart well beyond the right sternal edge, with 
moderate horizontal extension of the cardiac area toward the left 
midclavicular line. On auscultation a more or less faint, abbreviated, 
sharply valvular tricuspid first sound is audible, and at the base the 
pulmonic second sound is enfeebled and obscure. The systolic 
bruit of relative tricuspid incompetence, with its striking attendant 
phenomena of venous stasis, is not unlikely to be a dominant physical 
sign, confirmative of the foregoing findings. 

Auricular Dilatation. — The physical signs of this condition have 
been referred to on page 423, under its attendant change, auricular 
hypertrophy. In this connection it may be added that in the study 
of auricular enlargements the venous pulse tracing is most helpful 
in determining to what extent and in what manner the integrity and 
power of these cardiac chambers have become affected. 

Diagnosis. — The diagnosis of cardiac dilatation rests upon the 
following distinctive signs: a feeble, wavy precordial impulse, an 



DISEASES OF THE CARDIOVASCULAR SYSTEM 429 

ill-defined, displaced apex-beat, a small, rapid, irregular arterial 
pulse, enlargement of the cardiac outline, and a weak though sharp 
first sound with an enfeebled second sound. The other evidence, 
relating to failing compensation and to back pressure and its conse- 
quences, is detailed in connection with valvular defects (see p. 444). 
and therefore need not be reconsidered here. 

Dilatation and hypertrophy, save for the enlargement of the cardiac 
area common to both, are attended by diametrically opposed physical 
signs, as enumerated at length above. In attempting to judge which 
process predominates in an example of combined hypertrophy and 
dilatation, one should be guided mainly by a minute analysis of the 
cardiac sounds, by the presence or absence of relative regurgitant 
murmurs, by the condition of the arterial and venous pulses, and by 
a study stasis of phenomena. Pericardial effusion has been contrasted 
with dilatation of the heart on page 412. 

MYOCARDITIS (Carditis; Granular Myocardial Degeneration; Myo- 
cardial Fibrosis; Myocardial Abscess) 

Clinical Pathology. — Acute Myocarditis. — Under acute diffuse 
inflammations of the myocardium it is convenient to include in one 
group certain degenerative processes primarily affecting the muscular 
fibers, and in another group acute inflammations of the interstitial 
tissue, the former being designated as parenchymatous, and the 
latter as interstitial, myocarditis. 

Acute parenchymatous myocarditis is to every intent and purpose 
identical with the condition known as " cloudy swelling " or "granular 
degeneration" of the heart, in which the muscular fibers become 
swollen, lose their striation, and are loaded with albuminoid granula- 
tions, the heart muscle in consequence acquiring a dull gray appear- 
ance and an abnormally soft and edematous consistence. A slight 
degree of interstitial inflammation usually attends this predominant 
parenchymatous change, which, if unchecked, inevitably leads to fatty 
degeneration. Parenchymatous inflammation of the myocardium, 
toxic in origin, is a familiar cardiac complication in many active 
febrile and infectious states — i. e., septicemia, enteric fever, pneu- 
monia, rheumatic fever, scarlatina, gonorrhea, influenza, and insola- 
tion; it arises in connection with exhausting cachexias; and it is 
sometimes consequent to endo- and pericarditis. 

Acute interstitial myocarditis, also referable to acute infections and 
to inflammations of the endo- and pericardium, consists of an infil- 
tration of the interstitial tissue with small round cells and leukocytes, 
together with vascular dilatation, and a variable degree of degenera- 



430 PHYSICAL DIAGNOSIS 

tion of the muscular fibers. This produces unnatural softening and 
grayish discoloration of the heart, either uniformly or locally, depend- 
ing upon whether the inflammation is diffuse or circumscribed. A 
mild interstitial myocarditis may undergo perfect resolution, leaving 
the cardiac muscle undamaged, but severe cases probably terminate 
in unalterable fibroid myocarditis. 

, Acute suppurative myocarditis is generally due to the lodgment of 
infected thrombi in the branches of the coronary artery, less commonly 
to the direct extension of a pyogenic lesion of the endocardium or 
the pericardium. Various septic processes, such as malignant endo- 
carditis, osteomyelitis, septic phlebitis, and puerperal fever, are the 
primary factors of this grave condition. The suppurative foci range 
in size from minute miliary points to abscesses as large as a centimeter 
or more in diameter, and may be either widely disseminated through 
the entire myocardium or restricted and circumscribed, notably to 
the anterior wall of the left ventricle. If small and few, the pus foci 
may become inspissated, absorbed, and cicatrized or calcified, but 
if there be extensive suppuration, and the subject survives, aneurism 
of the cardiac wall is a possible sequel. Or the pus may penetrate the 
pericardial sac or ulcerate into one of the cavities of the heart, exciting 
in the former instance fatal purulent pericarditis, and in the latter, 
metastatic abscesses of remote organs contaminated by septic emboli 
carried by the ventricular blood streams. An interseptal abscess 
may, by erosion, establish a communication between the ventricles 
or the auricles. 

Chronic Myocarditis. — This type of heart disease, most common 
in men of middle or advanced age, consists of a chronic interstitial 
inflammation of the myocardium terminating in fibroid induration. 
Usually the process is chronic from its inception, but sometimes 
it is the sequel of an acute myocardial inflammation or degeneration. 
Disease of the coronary arteries is undoubtedly the leading factor of 
chronic myocarditis, which ordinarily is the result of the nutritive 
defects consequent to obliterative endarteritis, although occasionally 
an area of anemic necrosis, referable to arterial thrombosis, is the 
starting-point of the lesion. In other cases the myocardial changes 
are due to the direct extension of chronic endocarditis or pericarditis, 
with predominant implication of the papillary muscles in the former 
event and of the outer surface of the myocardium in the latter. 
Fibrosis of the heart muscle is part and parcel of the retrograde 
changes incident to advanced age; it is excited by the irritant action 
of circulating toxic substances, as in rheumatic fever, malarial fever, 
syphilis, and as in alcoholism, nicotin-poisoning, plumbism, gout, 






DISEASES OF THE CARDIOVASCULAR SYSTEM 43 1 

diabetes, and nephritis; it develops after various acute infectious 
diseases, doubtless as a sequel of a primary interstitial myocarditis 
of intense grade; and, most exceptionally, it arises traumatically, 
as from an injury to the precordia. 

The fibrosis may be so extensively distributed as to merit the term 
diffuse, or, as is more frequently the case, it may be more or less 
restricted, especially to the apical portion of the left ventricular wall, 
to the interventricular septum, and to the papillary muscles; in 
congenital cardiofibrosis, however, the apex of the right ventricle is 
the favorite site of the lesion. The affected areas are recognized 
as linear stripes and rounded patches of grayish-white induration, 
composed of connective-tissue bands paralleling the muscle-fibers, 
which eventually atrophy, undergo granular and fatty degeneration, 
and perhaps become wholly obliterated, in consequence of com- 
pression by the overgrowth. In rheumatic myocarditis the myo- 
cardial nodules of Aschoff are commonly found, existing as discrete 
microscopic areas of leukocytes and embryonal tissue, tending 
ultimately to form scars, and situated usually in the subendocardial 
parts of the septum in the left ventricular wall. 

Associated changes of myocardial fibrosis include pressure stenoses 
of the aortic and pulmonary orifices produced by cicatricial contrac- 
tions; mitral and tricuspid leakages due to fibroid shortening of the 
papillary muscles; chronic valvulitis and pericarditis; and obliter- 
ative endarteritis of the coronary vessels. Hypertrophy and dila- 
tation are common sequels, but of these changes the attendant 
arteriosclerosis, valvular defects, and pericarditis are also im- 
portant factors; or hypertrophy may occur merely as a com- 
pensatory overgrowth of the non-fibrous parts of the muscle. 
In cases of advanced myocardial disease there is a tendency toward 
thrombosis within the chambers of the heart, particularly in the 
auricular appendages and in the ventricles near the apex. Aneu- 
rism of the heart may arise if a circumscribed patch of fibrosis 
becomes so weakened by degenerative changes that finally it 
yields and bulges under the incessant strain of intracardiac 
pressure. 

Finally, there is a large group of cases bearing every clinical hall- 
mark of chronic myocarditis which at necropsy show no lesion 
whatever of the heart muscle, endocardium, valves, or coronary 
vessels. In these instances, despite the absence of inflammatory 
and degenerative changes, one must assume the existence of car- 
diac failure due to myocardial insufficiency, and for all practical 
purposes such an assumption is entirely justified. As Christian 



432 PHYSICAL DIAGNOSIS 

points out, these examples of cardiac insufficiency and decompensa- 
tion without demonstrable changes in the muscle and valves are 
called myocarditis by the clinician, although the term does not 
necessarily mean inflammation of the myocardium, as recognized 
by the pathologist. 

Physical Signs. — Inspection. — In acute forms of the disease the 
patient's pallor, apathy, and breathlessness constitute a most sug- 
gestive trio of objective signs, or there may be a cyanotic counte- 
nance which betrays a lagging circulation. Subjects of myocardial 
fibrosis are notably affected by shortness of breath and distressing 
palpitation upon slight exertion. In suppurative myocarditis one 
should look for profound depression, collapse, symptoms of sepsis, 
and evidences of septic infarcts; and precordial pain is not un- 
usual in this type of myocardial inflammation. 

Palpation. — Enfeeblement of the cardiac impulse and a forceless, 
empty, and often arhythmic pulse-beat are discovered by precordial 
and radial palpation, and, if there be considerable venous stasis, 
the liver and the spleen become palpably enlarged. In chronic cases 
a slow pulse is the rule, except in the event of advanced fatty changes 
or dilatation, which provoke undue rapidity and weakness of the beats. 

Percussion. — Unnatural extension of the cardiac area, particularly 
in a horizontal direction, is found in cases associated with decided 
dilatation of the heart, but, naturally, this helpful clue to the recogni- 
tion of the myocardial damage is forthcoming only in advanced 
cases. 

Auscultation. — The tones of the heart are enfeebled, muffled, and 
impure in accordance with the gravity of the existing cardiac asthenia. 
Ordinarily the muscular sound is indistinct or even inaudible, so that 
the valvular quality of the heart's sounds predominates; or, as 
sometimes happens, the valvular tone, too, is suppressed, in which 
event it is difficult to auscultate any distinct cardiac sounds whatever. 
The systolic murmur of a relative mitral leakage, from stretching 
of the valve ring, is not uncommonly audible at the apex, and, should 
endocarditis or pericarditis coexist, the adventitious sounds of these 
complications are also appreciable. 

Diagnosis. — Acute myocardial degeneration is the natural inference 
when, during the course of an acute infectious process, dyspnea, 
pallor, vomiting, and precordial oppression and distress supervene, 
along with a rapid pulse of low tension and a muffled impurity of 
the cardiac sounds. The discovery of a systolic (relative) murmur 
at the apex, of the percussion findings of ventricular dilatation, and 
of evidences of venous stasis change such an inference to a reasonable 



DISEASES OF THE CARDIOVASCULAR SYSTEM 433 

certainty. Suppurative myocarditis, though rarely diagnosed cor- 
rectly during life, is suggested by extreme severity of the constitutional 
symptoms, by the existence of a septic etiologic factor, and by the 
occurrence of embolic processes. 

Chronic interstitial myocarditis is prone to affect middle-aged men 
whose arteries have become sclerotic from the immoderate use of 
alcohol or from the effect of syphilis, gout, or similar poisons to the 
cardiovascular system. Or it may attack the clean-lived man of 
affairs long subject to the stress of a strenuous business or pro- 
fessional routine. In such subjects the important diagnostic 
details consist of hardening of the palpable arteries; a persistently 
high-tension pulse commonly deviating from the normal rate and 
rhythm; a comparatively feeble first apical sound of valvular quality 
and perhaps masked by a systolic murmur of mitral leakage; ringing 
accentuation of the aortic second sound, not infrequently attended 
by a systolic murmur of aortic atheroma and dilatation; and extension 
of precordial flatness indicative of enlargement of the left ventricle 
and of the ascending part of the aorta. In advanced cases the 
supervention of dilatation may transform the foregoing picture into 
one of cardiac breakdown. Other evidences, of arteriosclerotic 
character, that may be associated with the cardiac signs comprise 
interstitial nephritis, glycosuria, anginal paroxysms, intermittent 
lameness, and certain cerebral symptoms, such as vertigo, recurrent 
attacks of transient aphasia, palsy, and, exceptionally, of the Stokes- 
Adams syndrome — bradycardia, syncope, and convulsions. 

ACUTE ENDOCARDITIS (Valvulitis; Acute Mural Endocarditis) 

Clinical Pathology. — Acute inflammation of the endocardium, 
implicating chiefly the valves but to a less extent the mural serosa, 
may occur clinically as a simple benign type or as a malignant process. 
In this connection, however, one should recall Osier's assertion, that 
"so-called benign endocarditis kills in the long run a very much 
larger number of persons than the malignant form, " for endocarditis, 
if it be not immediately perilous, tends to become so ultimately, in 
consequence of the sclerotic changes thereby provoked. Further- 
more, there is no clear-cut pathologic demarcation between the two 
forms of inflammation, since they represent but different grades of 
intensity of the same infectious process. 

Rheumatic infection is par excellence the factor of acute endocar- 
ditis, and the vast majority of instances are traceable to this poison, 
either in its frank arthritic form or in some one of its guises — 
28 



434 PHYSICAL DIAGNOSIS 

tonsillar, choreic, or cutaneous. Conservatively, it is safe to be- 
lieve that in adults rheumatic affections inflame the endocardium 
in fully one-half of all cases, and that in children this incidence is 
greater. Of Cowan's compilation of 1750 cases of acute rheu- 
matic fever, 933 showed endocarditis, or 53.3 per cent. Other 
causes that may light up an endocarditis include certain sep- 
tic and pyemic processes: erysipelas, gonorrhea, osteomyelitis, 
puerperal fevers, infected wounds, abscess; and many of the 
specific fevers, such as pneumonia, diphtheria, scarlatina, influenza, 
tuberculosis, and, less commonly, other infectious and eruptive 
diseases. As a terminal infection there is no doubt that a mild grade 
of endocardial inflammation commonly develops, nor is there any 
doubt that traumatism, unless attended by bacterial invasion, never 




Fig. 1650. — Electrocardiogram of a case of acute endocarditis, showing deep Q- 
depression, large i?-wave, inverted T-wave, and irregular prolongation of T, R interval. 
(Tracing by. Dr. T. A. Cope.) 

excites a vegetative endocarditis. Valve leaflets habitually exposed 
to the irritant effect of arterial hypertension are particularly prone 
to become inflamed and vegetative. The streptococcus, staphylococ- 
cus, pneumococcus, and gonococcus are the germs that have an 
especially close causal relation to endocarditis, while less commonly 
the lesion is excited by such bacteria as the bacillus of tuberculosis, 
influenza, or enteric fever, or by some other specific microorganism. 

Simple acute endocarditis, as a rule, attacks the valves of the left 
side of the heart, the mitral, aortic, tricuspid, and pulmonic structures 
being affected in the order of frequency named. Lesions of the right 
side of the heart are generally of intrauterine origin, but it is proba- 
ble that right-sided endocarditis during postuterine life is not such a 
rarity as was once supposed, though signs of such a condition are not 
frequently found, owing to the relatively greater tendency of reso- 
lution to occur in lesions of the tricuspid and pulmonic valves (v. i.). 

Simple acute endocarditis has a special predilection for the lines 



DISEASES OF THE CARDIOVASCULAR SYSTEM 435 

of valve contact a short distance (about yV inch or 2 mm.) from 
the free margins, the auricular surface of the mitral leaflets and 
the ventricular aspect of the aortic cusps usually showing the 
earliest and most advanced alterations, which are primarily those 
of endothelial degeneration and are structurally of thrombotic char- 
acter. The affected valves are the seat of local endothelial necroses, 
the swollen, abraded, and roughened surfaces becoming covered 
with a deposit of granular or fibrillar fibrin permeated by proliferating 
connective tissue and by infiltrated leukocytes. The vegetations 
developed in this manner appear as delicate or as coarse excrescences 
attached to the valves, and, if recent, of pinkish color and friable 
texture, or, if old, pale and of hard, warty consistence. Such vegeta- 
tions, if small, soft, and delicately globular, merit the term beaded 
excrescences; those of greater size, denser character, and cauliflower- 
like or warty in form are well described as verrucose excrescences; 
and those of inordinate size and polypoid contour are referred to as 
villous or polypous lesions. The tissues of the affected valves show 
more or less inflammatory damage, leading to a corresponding 
degree of thickening, contraction, and puckering of the leaflets, 
whereby orificial stenosis and incompetence arise. Rarely, a simple 
acute endocarditis of the benign type undergoes resolution and leaves 
the valve functionally perfect; or it may undergo extensive necrotic 
and ulcerative changes; but ordinarily it results in the unalterable 
structural deformities distinctive of chronic valvular disease. The 
detachment of a valve thrombus or of a bit of necrotic tissue is a 
cause of embolism. Apart from the local lesion, acute endocarditis 
sets up a variable grade of myocardial inflammation and degenera- 
tion, which, indeed, may do more harm than the valvular defects. 
Pericarditis is also a familiar associated lesion — Sturges found it in 
94 per cent, of cases in children, and in view of the frequency with 
which endo-myo-pericarditis coexists he purposes to apply the 
term carditis to the majority of acute endocardi tides; or the term 
pancarditis, suggested by Jiirgensen, seems even more appropriate. 
Laceration of a valve, rupture of a tendinous cord, aortitis, pleuritis, 
and pneumonitis are other possible complications, the first three 
being most exceptional. 

Ulcerative or malignant endocarditis is generally due to strepto- 
coccal, staphylococcal, pneumococcal, or gonococcal infection, and, 
though commonly left sided, implicates the right heart more fre- 
quently than does simple benign endocarditis. The process is one 
of predominant necrosis and of subordinate repair, leading to exten- 
sive and irreparable structural damage. This may take the form of 
ulcerative erosion resulting in more or less complete destruction of 



436 



PHYSICAL DIAGNOSIS 



one or more valve cusps , in valve fenestration and aneurism, and 
in rupture of chordae tendineae; or ulcers may perforate a valve 
ring, produce septal perforation, and, penetrating the mural endo- 
cardium, set up a suppurative myopericarditis, perhaps terminating 
in cardiac aneurism or in rupture of the heart. Septic embolism 
is a grave danger associated with a mycotic process of this sort. In 
other cases the ulcerative changes are overshadowed by the formation 
of luxuriant vegetations springing from the valve mechanism and 




Fig. 166. — Malignant endocarditis, with extensive implication of aortic valves (Phila- 
delphia General Hospital). 

from the mural endocardium, the vegetative outgrowths commonly 
being attended by deep necrosis. If not leading to an immediately 
fatal outcome, the excrescences sometimes proliferate to a most 
extraordinary extent and ultimately may become coated with an 
unyielding, rigid deposit of lime salts. 

Physical Signs. — Inspection. — In the average case of simple 
endocarditis there are no visible evidences of the lesion, unless, as 
exceptionally happens, the myocardial damage is grave enough to 



DISEASES OF THE CARDIOVASCULAR SYSTEM 437 

displace the apex-beat and to alter its force. It is in malignant cases 
particularly that signs of cardiac dilatation are likely to be observed, 
and in these instances the subject may show the inroads of profound 
septic poisoning. 

Palpation. — Suggestive, but by no means characteristic, informa- 
tion is occasionally afforded by palpation. So long as myocardial 
integrity is unimpaired palpation, of course, shows nothing, but in 
the case of an acute valvulitis grafted upon an old valvular lesion 
abnormal variations in the force, extent, and site of the apex-beat, 
sometimes a thrill, and perhaps hepatic enlargement are to be looked 
for. The pulse is commonly increased in frequency, especially in feb- 
rile subjects, and maybe altered in volume, in tension, and in rhythm. 

Percussion. — Routine percussion of the cardiac areas, particularly 
those overlying the ventricles, is indicated in every suspected case of 
endocardial inflammation, irrespective of its benignancy or malig- 
nancy, in order thus to be able to detect the first indications of 
ventricular dilatation. In the absence of this change the percussion 
findings indicate no alteration in the extent of the normal cardiac 
outline. 

Auscultation. — The earliest definite physical sign of simple acute 
endocarditis, in the gieat majority of instances, consists of an impurity 
of the first cardiac-sound at the apex, followed by a muffled prolonga- 
tion of the tone, and finally succeeded by the development of a 
distinct, though usually soft and blowing, systolic murmur w T hich is 
clearly conducted as far as the patient's axilla, and in time is attended 
by accentuation of the pulmonic second sound. This transition from 
a murmurish tone to an actual bruit having a well-defined area of 
propagation points to mitral regurgitation, the most common con- 
sequence of this type of endocardial disease. Less commonly, a 
muffled aortic second sound similarly is converted into a diastolic 
murmur, or the rough bruit of mitral stenosis may appear. The 
mere presence of a murmur, especially if it be basal, does not mean 
endocarditis, for such a sound is quite as likely to be anemic or 
relative as it is to be endocarditic. The criterion, then, is not the 
murmur, so much as the sequence of tonal changes attending its 
development. Furthermore, the inability to hear a murmur does 
not exclude valvulitis, which, if it does not fulfil certain physical 
conditions, creates no vibrations of the blood column. 

Malignant endocarditis may afford auscultatory signs identical 
with those of the benign form, or there may be none at all. In certain 
cases, however, characterized by extensive and highly virulent endo- 
cardial damage, there are single or multiple murmurs peculiar in 
their tendency to change in puncta maxima, and in rhythm, intensity, 



438 PHYSICAL DIAGNOSIS 

and quality, affecting, as they do so, the character of the other cardiac 
sounds. To a single mitral murmur, for example, may suddenly 
be added an aortic bruit, as the mycotic process bridges the short 
endocardial path separating the two orifices. Myocardial impair- 
ment of the cardiac tones, the dry rub of pericardial inflammation, 
and the friction- sound of pleurisy are important consecutive findings 
in malignant infection of the endocardium. 

Diagnosis. — In acute simple endocarditis the gradual supervention 
of a murmur attended by undue intensity of the pulmonic second 
sound and by signs of myocardial weakness is the chief diagnostic 
clue, which, unfortunately, is not available in every case. Due 
attention must also be paid to other suggestive clinical findings, such 
as moderate fever, rapidity of the pulse, precordial uneasiness 
(rarely, actual pain), and more or less respiratory oppression; while 
the patient's history, present and previous, is to be interrogated 
with a view to finding some factor of endocardial inflammation — 
rheumatism, tonsillitis, pneumonia, or similar infectious process. 
The distinction between true endocarditic murmurs and the adven- 
titious sounds due to anemia, to relative incompetence, and to plastic 
pericarditis is considered at sufficient length in connection with these 
conditions. (See pp. 387 and 399.) 

In certain cases of malignant endocarditis the development of 
erratic, changeable murmurs and of cardiac dilatation in an unmis- 
takably septic subject provides satisfactory evidence of an endo- 
cardial ulceration. But in cases that do not conform to this cardiac 
type the local signs may be most equivocal, so that one must turn 
elsewhere for definite data, which in general refer to a condition of 
septic poisoning and in particular to pyemia, co the typhoid state, 
and to meningeal inflammation, according to the existing individual 
peculiarities. In studying such a varied symptomatology it is 
important first to discover the presence of some septic factor, either 
local or general, and to identify, by blood-culturing, the infective 
agent, after which investigation of the systemic damage wrought 
thereby is in order. This inquiry should be directed toward the 
presence or absence of chills, remittent pyrexia, progressive anemia, 
rapid wasting, extreme exhaustion, splenic enlargement, leukocyto- 
sis, iodophilia, and evidences of septic embolism. There is also a 
puzzling group of cases that shows little else than moderate, often 
recurrent, fever and splenic enlargement, together with clear signs of 
chronic valvular disease. These cases, which may be acute, chronic, 
or relapsing in type, are especially liable to embolic accidents, and 
probably represent an active necrotic process implanted upon a 
preexisting valvular sclerosis. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 439 

Enteric fever may closely resemble malignant endocarditis, in 
general symtomatology and in the existence of an endocardial 
(relative) murmur. Apart from the patient's previous history, these 
data bespeak typhoid: prodromal indisposition, gradual onset 
without a true rigor, relatively late prostration, specific findings 
from blood-cultures and from the serum test, and the orderly appear- 
ance of the distinctive symptom-complex of enteric fever by the end 
of the first week. 

Malarial fever, although it may superficially ape malignant endo- 
carditis, can scarcely prove a source of serious confusion, in the face 
of its distinctive hematologic picture — leukopenic mononucleosis, free 
pigment, and the malarial hemameba. 

CHRONIC ENDOCARDITIS (Chronic Valvular Disease; Chronic 
Interstitial Endocarditis) 

Clinical Pathology. — Chronic inflammation of the valvular and 
mural endocardium occurs both as a sequel of acute endocarditis 
and as a primary chronic sclerosis, in either event leading to de- 
formities of the valves and orifices whereby regurgitant and stenotic 
lesions arise, and also to permanent alterations in the structure and 
functional efficiency of the cardiac muscle. More than one-half 
of all chronic valvular defects are traceable to rheumatic poison, 
and especially in childhood and in young adult life is this irritant 
the cause of the original endocardial inflammation. Langmead 
found signs of endocarditis in 87 per cent, of 133 rheumatic school 
children, and in approximately 3 per cent, of 2556 children ex- 
amined, regardless of their past medical history. 

Less commonly the permanent lesions are due to an acute 
endocarditis excited by some one of the numerous other factors 
referred to above. In the type of chronic valvular disease arising 
as a slow fibrosis the damage generally can be laid at the door of 
alcohol, syphilis, and muscular strain, which, singly or in combina- 
tion, subject the valve mechanism to irritation by circulating toxins 
and by excessive arterial tension. Arteriosclerosis, nephritis, gout, 
malaria, diabetes, and plumbism act similarly. 

The special manner in which the different valves are affected by 
chronic endocarditis and the important secondary cardiac changes 
thereby set up are, for convenience sake, considered in connection 
with the several types of individual valvular lesions. (See p. 446 
et seq.) It is sufficient here to summarize the pathologic findings 
of chronic valvular disease as follows: (a) Fibrosis, induration, and 
thickening of the valves and of their musculotendinous attachments; 
(b) contraction of the hyperplasia, resulting in curling and puckering 



44° PHYSICAL DIAGNOSIS 

of the valve edges, shortening and thickening of the chordae tendineae 
and papillary muscles, and orificial deformity, whereby faulty 
approximation of the cusps arises; (c) adhesion of the valve edges, 
restricting their movements and causing obstruction and leakage at 
the orifices they guard; (d) impregnation of the sclerotic structures 
with lime-salts, still further adding to their rigidity and mechanically 
interfering with their normal movement; (e) sclerotic thickening 
and calcification of the mural endocardium. The valves thus 
damaged are sometimes found to be beaded with simple inflammatory 
excrescences, and are prone, in the event of bacterial invasion, to 



Aortic 

III. Regurgitation 

IV. Stenosis 




Mitral 

I. Regurgitation 

II. Stenosis 



Fig. 167. — Relative incidence of regurgitant and stenotic lesions of the mitral and 

aortic valves. 



become attacked by a malignantly necrotic process, or, if exposed to 
sudden violent strain, may rupture. Myocardial degeneration and 
inflammation are practically constant associated lesions which, as 
intimated before, give more concern to the clinician than do the 
underlying valvular defects. 

Types and Relative Incidence of Valvular Lesions. — A valvular 
defect acting as a barrier to the onward flow of blood is known as 
a stenosis, or an obstruction, and a deformity preventing the tight 
closure of a valve, and thus permitting backward leakage through 
the orifice into the chamber immediately behind, is designated as a 
lesion of regurgitation, incompetence, or insufficiency. Valvular 
lesions may be single, but more commonly they are either double or 



DISEASES OF THE CARDIOVASCULAR SYSTEM 44 1 

combined, a single lesionbeing either stenosis or regurgitation of one 
orifice, a double lesion meaning both stenosis and regurgitation at 
one orifice, and a combined lesion consisting of two or more defects 
at different orifices. 

The valves of the left side of the heart are much more frequently 
implicated than those of the right side, defects of the tricuspid and 
pulmonic leaflets usually arising as sequels of left-sided disease, and 
but exceptionally representing acquired primary processes. Con- 
genital valvular disease is right sided in the vast majority of instances. 
Mitral regurgitation is by all odds the most common single valvular 
defect, after which follow, in this order of frequency, mitral stenosis, 
aortic regurgitation, 1 and aortic stenosis (Fig. 167). The relative 
incidence of organic right-sided defects reads: tricuspid regurgi- 
tation, tricuspid stenosis, pulmonary stenosis, and pulmonary regurgi- 
tation. Of combined lesions, F. J. Smith has worked out this order 
of frequency: double aortic and mitral regurgitation; aortic and 
mitral stenosis; aortic and mitral regurgitation; double aortic and 
double mitral. • 

The comparative frequency of valvular defects at the four different 
cardiac orifices is illustrated by the following table, based upon the 
analysis of nearly 4000 collected cases: 

,,. , . .. Mitral and Pulmonic 

Lockhart Gillespie. Mttrai. Aortic. ^^ Tricuspid. 

(1914 cases.) 58.5 per cent. 21.4 per cent. 19.2 per cent. 0.8 per cent. 
T. G. Ashton. 

(1024 cases.) 60.6 " 21.5 " 17.0 " 1.0 " 
Parrot. 

(1058 cases.) 58.6 " 35.9 " 0.5 

From other data given by these and other authors, notably F. J. 
Smith and Middleton, too elaborate for quotation here, these general 
facts relating to chronic valvular disease may be deduced: 

1. Including both sexes, mitral disease constitutes more than 
one-half of all cases; in men less than one-half, and in women more 
than three-fourths of valvular lesions are mitral. 

2. Including both sexes, aortic disease constitutes about one-fifth 
of all cases; it is three times as common in men as it is in women. 

3. Double or combined lesions are found in about one-fifth of 
all cases; they are almost twice as common in men as in women. 

4. Right-sided lesions constitute less than one one-hundredth of 
the total cases of valvular disease. 

1 It is, perhaps, questionable which of these two defects is the more common, 
for their incidence is practically about the same. Most statistics, however, 
show that mitral stenosis is a shade the more frequent. 



442 PHYSICAL DIAGNOSIS 

Primary Effects of Valvular Lesions. — In health the blood flows 
unimpeded through the chambers o.^ the heart into the arterial, 
capillary, and venous channels, and thence back into the heart. 
Not only does the stream always flow in the same direction, but with 
each systole exactly the right volume of blood is emptied into the 
arterial system by the contracting ventricles, to maintain perfect 
circulatory equilibrium. This is ensured so long as the valves 
open and close properly and the size of the orifices remains normal, 
but the balance is immediately disturbed when valvular defects 
develop, which either obstruct the onward flow of the blood-stream 
or permit its reflux. 

Valvular defects, whether they obstruct the blood-stream or allow 
it to regurgitate, primarily cause accumulation and stasis of blood 
in the chamber of the heart immediately back of the crippled valve, 
with the result that this chamber becomes habitually overdistended 
and dilated. The muscular walls then hypertrophy, in consequence 
of the increased work demanded of them, but ultimately they again 
tend to dilate, as they sooner or later weaken under the continued 
strain. The chamber primarily affected then gives out completely, 
and the back pressure extends to the other parts of the cardiovascular 
system, step by step. The predominance of one or the other of these 
structural changes in the cardiac muscle depends upon the peculiar- 
ities of the determining lesion and upon the extent and character of 
the retrograde changes in the myocardium. These influences will 
be discussed presently, in connection with the individual valvular 
lesions. 

A condition of compensation is said to exist so long as the heart 
adequately responds to the demands made upon it to overcome, by 
increased work, the stress imposed by valvular defects. Thus, by 
virtue of its reserve force, the heart enlarges so as to equalize the 
circulatory disturbance by overcoming the stasis, and the conservative 
change, compensatory hypertrophy, supervenes (Fig. 168, //). Perfect 
compensation continues so long as the nutrition of the myocardium 
is sufficient to allow the development of hypertrophy adequate to 
maintain a normal cardiovascular equilibrium, and at this stage of 
a valvular disease the cardiac physical signs are the sole evidences of 
the lesion to be detected. It is important to bear in mind the fact 
that during this period of perfect compensation drugs are not only 
not indicated, but their use may be distinctly injurious, no matter 
what be the character of the cardiac defect. 

Decompensation {ruptured or broken compensation) supervenes 
when the nutrition and reserve force of the heart fail to keep pace 
with the strain imposed by the valvular lesion, so that the circu- 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



443 



latory balance becomes disturbed and the stasis aggravated. It 
is a change referable to myocardial enfeeblement and ultimate 
dilatation of the heart which develops, either gradually or ab- 
ruptly, when the nutrition of the heart becomes so impaired that 
this muscle relaxes under the stress which hitherto it has been able 
to bear, and hence the total available cardiac force is inadequate 
for the maintenance of the normal circulatorv balance (Fig. 168, 

Muscular insufficiency of the heart, therefore, is the prime factor 
of "heart failure," and upon the integrity of the cardiac muscle de- 
pends the prognosis in the individual case, independent of the 
nature of the valvular defect, the character of irregularities, and the 
degree of hypertrophy. It is essential to bear in mind this basic 
premise in the study of the heart, and not to subordinate it to 
signs afforded by murmurs and by instrumental records of the 
pulse and the blood-pressure. 



Tone required, 
to preserve 
Compensation. 




Hypertrophy 
K&eroe Force. 

Reserve T^ree. 



Ordinary 
force- 




Fig. 168. — The effects of adequate and of ruptured compensation upon the force 
of the heart: I, Normal cardiac force; 77, excess of cardiac force attending stage of 
adequate compensation; III, deficiency of cardiac force incident to stage of ruptured 
compensation. 

Ruptured compensation is betrayed not so much by distinctive 
cardiac physical signs as by groups of symptoms, more or less urgent, 
indicating circulatory derangements in different organs. For 
example, in left-sided valvular disease the brunt of the strain is felt 
by the lungs which become engorged as soon as the stasis and high 
tension extend backward from the left auricle and reach the 
pulmonary circulation. Later the congestion, via the pulmonary 



PHYSICAL DIAGNOSIS 



ait, affects the right side of the heart, and ultimately extends 
even beyond its confines into the vena? cava?, causing general 
venous engorgement. 

SecoK-fcry Ejects of Valvular Lesions. — The secondary effects of 
valvular disease develop in consequence of the back pressure of blood, 



5u:::-vi- vein 



^ Subclavian artery 



F'_'~:~:.ry irtery 



PulncrLirv veins 




— Renii ir:ery 
G_s-i: .:_r:er:e< 



r-'.ri:: r.i:; 



Inferior mesenteric 



Iliac reins 

Fig. 169. — Mechanism of the stasis phenomena 

disease. 



to chronic valvular 



which in course of time causes venous congestion of different organs 
and parts of the body remote from the crippled heart. These sign? 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



445 



of stasis are referred to the respiratory system, the gastro-intestinal 
tract, the kidneys, the brain, and the great venous trunks. The 
mechanism by which these changes arise is illustrated in the accom- 




Fig. 170. — Appearance of a subject of chronic valvular diseas 
failing compensation (Jefferson Hospital). 



ing the stage of 



panying diagram (Fig. 169), and their recognition may be facilitated 
by referring to the following symptom-groups: 



Bronchopulmonary: 



Castro-intestinal: 



Renal: 
Cerebral: 



Venous: 



Cough; dyspnea; orthopnea; hemoptysis; bronchitis; 
edema of lungs; passive congestion of lungs; hydro- 
thorax. 

Chronic gastric and intestinal catarrh; hemater. 
melena; hemorrhoids. 

Enlarged, tender, and pulsating liver; icterus. Enlarged 
and tender spleen. 

Urine scanty, high specific gravity, high color, and con- 
taining albumin, urates in excess, and tube casts. 

Headache; vertigo; faintness; syncope; phosphenes; 
insomnia; unpleasant dreams; drowsiness; delirium. 

Embolism; thrombosis; cerebral hemorrhage. 

Cyanosis of face and extremities; clubbed fingers, 
tolic jugular pulsation. Edema of extremities; ascites; 
anasarca. 



446 



PHYSICAL DIAGNOSIS 



The special pathology, physical signs, and diagnosis of the several 
varieties of chronic valvular disease will now be considered with 
relation to the individual lesions. 



MITRAL REGURGITATION 

Clinical Pathology. — This, the most common of all organic 
valvular lesions, is usually acquired during childhood, doubtless 
because at this period of life factors of endocarditis, such as rheuma- 
tism, chorea, tonsillitis, the exanthemata, and other infections, are 
prevalent. Less commonly leakage at the mitral orifice depends 
upon arteriosclerotic changes supervening in later life, as the result 
of nephritis, gout, syphilis, or the habitual use of alcohol. Traumatic 

Deformed mitral valve 




Fig. 171. 



Cavity of left auricle 
-Mitral regurgitation (Jefferson Hospital Laboratories). 



injury of the valve is a potential source of mitral regurgitation, and 
congenital defects, in the exceptional instance, account for the 
incompetency. 

Interference with the accurate apposition of the mitral valve 
curtains results in imperfect closure of the mitral orifice, and, in 
consequence, leakage of blood from the ventricle into the auricle 
takes place during ventricular systole. This condition of mitral 
regurgitation is due fundamentally either to organic derangement of 
the valve mechanism or to muscular changes in the wall of the left 
ventricle, singly or combined. In the organic type (Fig. 171) 
endocarditic induration and contraction of the mitral leaflets, with 



DISEASES OF THE CARDIOVASCULAR SYSTEM 447 

endocarditic induration and contraction of the mitral leaflets, with 
thickening, eversion, and fusion of their edges and perhaps adhesion 
to the ventricular wall, are ordinarily responsible for the faulty 
closure of the mitral orifice. Or the latter may leak because the 
cusps are prevented from closing tight by vegetations upon their 
surface, by the projection of calcareous plates at their base, or by 
sclerosis and contraction of the mitral ring. In extreme examples 
the valvular structures at the mitral orifice are virtually converted 
into a dense calcareous mass, and in this event there is obviously 
stenosis as well as regurgitation at the auriculoventricular opening. 
The foregoing changes are attended by more or less shortening and 
fibrocalcareous degeneration of the tendinous cords and papillary 
muscles, which possibly may even rupture. Exceptionally a valve 
leaflet is the seat of laceration, fenestration, or so-called aneurism. 
In the muscular type the leakage is due not to structural damage to the 
valves but to enlargement of the auriculoventricular orifice and 
to defective muscular action incident to myocardial enfeeblement and 
dilatation of the left ventricle. Febrile conditions, anemia, and 
myocardial inflammation and degeneration, by interfering with 
cardiac nutrition, are likely to cause this type of degeneration, which 
also may arise in consequence of ventricular enlargement secondary to 
habitual arterial hypertension or to aortic valvular lesions. Relative 
incompetence develops as the result of left ventricular dilatation, the 
mitral orifice being so stretched that its valve curtains fail to close 
tightly, and the ventricular walls being so distended as to drag upon 
the musculotendinous attachments of the valve segments and hence 
to prevent their perfect approximation. It is likely that the 
reflux thus permitted, if adequately accommodated by the pul- 
monary circulation, relieves the stress of a laboring left heart, 
by a mechanism comparable to that of the well-known "safety- 
valve action" at the tricuspid orifice in distention of the right ven- 
tricle. (See p. 475-) Muscular incompetence also may occur 
primarily from feeble ventricular systole, a defect leading to 
insufficient constriction of the mitral orifice and to deficient 
action of the papillary muscles, by fault of which systolic back- 
ward leakage of blood is permitted through the inadequately 
guarded mitral orifice. 

As the result of mitral insufficiency both a normal supply of blood 
from the pulmonary veins and a reflux stream from the ventricle 
pour into and together overdistend the left auricle, which in con- 
sequence dilates, and, since expulsion of this large blood mass means 
additional effort, the auricular wall also undergoes compensatory 
hypertrophy. The left ventricle becomes similarly dilated and 
hypertrophied, for of necessity it must receive and expel an abnor- 



448 PHYSICAL DIAGNOSIS 

mally great volume of blood. As the result of the auricular sur- 
charging there are stasis and hypertension of the pulmonary circu- 
lation attended by dilatation, and, even by atheroma of the vessels, 
and finally, by brown induration of the lungs. By fault of the pul- 
monary engorgement the right ventricle is so strained and overworked 
that it dilates and hypertrophies, and when, after a variable period, 
the limit of hypertrophy is reached and dilatation predominates, 
the tricuspid valve leaks, permitting systolic regurgitation into the 
right auricle, which in turn dilates and hypertrophies in an endeavor 
to compensate the venous resistance. Hand in hand with this 
embarrassment of the right heart, systemic venous congestion pro- 
gresses, sooner or later to set up chronic catarrh of the mucosal 
surfaces, transudative accumulations in the serous sacs and subcu- 
taneous tissue, and visceral engorgement and induration. The car- 
diac muscle, meanwhile, enfeebled by the combined effects of under- 
nutrition and overwork, is the seat of fibrous and fatty degeneration. 

Physical Signs. — Inspection. — So long as the cardiac strength is 
adequate the patient's appearance is not suggestive of any valvular 
defect, but with the onset of venous stasis and failing compensation, 
dyspnea, cyanosis, especially of the lips, nose, and fingers, cough, 
watery or blood-streaked expectoration, and dropsy form a familiar 
group of objective symptoms. In cases of considerable chronicity 
one expects also to find more or less dilatation of the superficial veins 
of the face and upper chest, clubbing of the finger-tips, emaciation, 
and a facies picturing anemic pallor, an ashen-gray hue, or an icteroid 
staining. 

The cardiac impulse is unnaturally extensive, and displaced 
downward and to the left as the result of the left ventricular enlarge- 
ment, while if the right ventricle be hypertrophied there is visible 
epigastric pulsation. Exceptionally, in young children the hyper- 
trophy is sufficient to produce outward bulging of the precordia, but 
in adults no such deformity occurs. 

Palpation. — The impulse over the enlarged ventricles is either 
forcible and heaving or weak and undulatory, according to whether 
hypertrophy or dilatation predominates; over the liver there may be 
distinct pulsation, due in most instances to the violent impact of the 
right ventricle, but in some produced by the transmission of a systolic 
venous pulse. Palpation over or just above the cardiac apex some- 
times, but by no means constantly, appreciates a delicate systolic 
thrill, which is the tactile equivalent of the murmur heard on aus- 
cultation. In examples of extreme regurgitation it is sometimes 
possible to detect, by palpation of the chest-wall, diffuse pulsation 
of the lungs — the so-called "pulmonary pulse." 



DISEASES OF THE CARDIOVASCULAR SYSTEM 449 

The radial pulse, save perhaps for slight acceleration and hypo- 
tension, remains practically normal until the left ventricle fails, but 
when this happens the beats become notably deficient in volume, 
inordinately rapid, and irregular in rhythm and force. Ineffectual 
systole, or an occasional ventricular contraction too feeble to produce 
a radial impulse, is not infrequently detected by simultaneous palpa- 
tion of the precordia and the wrist. The sphygmogram of such a. 
pulse well illustrates its striking irregularity and low tension, the 
incidence of the curves being most erratic and their height unequal, 
with a vertical upstroke, sharp apex, rapidly falling downstroke, 
and low dicrotic wave. (See Fig. 130, in and vii; p. 348.) 

Percussion. — The area of cardiac dulness is increased horizontally 
and downward toward the left, owing to the bilateral ventricular 
enlargement, and occasionally it is possible to map out an upward 
extension of the basic outline corresponding to the situation of an 
enlarged left auricle. The size of the hepatic and splenic percussion 
areas is increased, as the result of venous obstruction. 

Auscultation. — Mitral regurgitation gives rise to systolic murmur 
at or near the apex, whence the sound is transmitted toward the left, 
usually into the axilla and sometimes as far backward as the inferior 
angle of the left scapula (Fig. 1 54) . The clear propagation of the 
sound toward the left depends upon the good conducting proper- 
ties of the chordae tendineae, the papillary muscles, and the ven- 
tricular wall, and upon the efficiency of the mural vibratory path 
formed by the chest-wall. 

Typically, the punctum maximum of this murmur is at the 
clinical apex of the heart, from which point the sound gradu- 
ally grows fainter as the stethoscope is moved beyond the limits 
of the precordia, but exceptionally the murmur is so loud as to be 
audible far beyond these confines. In rare instances a mitral systolic 
murmur is heard most distinctly along the left sternal border, usually 
between the fourth and sixth costal cartilages, but occasionally as 
high as the second interspace. The murmur of a mitral leakage is 
more likely to be soft and blowing than harsh or rasping, and its 
distinctness is decidedly affected by the subject's posture, the sound 
often being clearer when the patient is recumbent. The duration of 
the murmur is variable: it may absolutely coincide with the first 
sound, perhaps through only the first part of this period, or occur 
in the latter portion of systole, in which case a moderate grade of 
incompetence is suggested (Sahli) . The longer the bruit the more 
conspicuous its diminuendo character, and the shorter the sound 
the more pronounced its " whiffy" quality. 

The first sound at the apex is partly or wholly replaced by the 



450 PHYSICAL DIAGNOSIS 

attendant murmur, and within certain limits it is true that the 
greater the degree of the regurgitation the more effectually its bruit 
masks the first sound of the heart, which may, indeed, be quite 
inaudible. Accentuation of the pulmonic second sound, due to 
pulmonary congestion, is a valuable corroborative sign of mitral 
disease, while reduplication of the second sound at the cardiac base, 
from unequal tension within the two ventricles, is of some significance. 

Diagnosis. — A systolic apical murmur propagated toward the 
left axilla, accentuation of the second pulmonic sound, and bilateral 
ventricular enlargement are the cardinal signs of mitral regurgitation. 
These signs, unmistakable during the stage of compensation, are 
more or less obscured later, when cyanosis, dropsy, erratic action of 
the heart, and other signals of cardiac break-down dominate the 
clinical picture. 

In relative mitral leakage versus the organic type, the physical 
signs are often an uncertain guide, since if the mitral orifice be widely 
stretched by a dilated left ventricle, the thrill, murmur, and loud 
pulmonic second sound of an endocarditic reflux will be faithfully 
reproduced. Rosenbach's statement, that a late systolic murmur 
invariably means an organic structural defect of the left auriculo- 
ventricular opening, is helpful, but the clinical history, the question 
of secondary signs, and the subsequent behavior of the essential 
cardiac findings must largely mold the final decision. Most rela- 
tive mitral murmurs, however, are comparatively quiet, poorly 
conducted, evanescent, unattended by accentuation of the pul- 
monic second sound, and unaccompanied by congestion of the 
lungs and of the right heart. They commonly develop in debili- 
tated, anemic subjects during the course of some acute febrile in- 
fection or other exhausting disease that induces myocardial weak- 
ness, and the bruit completely vanishes when the tone of the 
cardiac muscle is restored. In a type of cardiac enfeeblement 
known as "Copenhagen heart" (Hielscher), common among ha- 
bitual users of strong snuff, relative mitral insufficiency is readily 
provoked by exercise, and frequently is accompanied by palpita- 
tion, dyspnea, and a rapid pulse of high tension. 

The murmur of aortic stenosis is sometimes audible at the apex, as 
well as at its punctum maximum at the aortic cartilage. But such 
a murmur, though timed like that of mitral regurgitation, usually 
has a harsh, rough tone clearly conducted into the carotids, and is 
accompanied by a basic thrill, by obliteration of the aortic second 
sound, and, not uncommonly, by a pulsus tardus or pulsus bisferiens. 

The distinctions between tricuspid regurgitation and a corre- 
sponding mitral defect are considered elsewhere. (See p. 397.) 






DISEASES OF THE CARDIOVASCULAR SYSTEM 45 1 

MITRAL STENOSIS 

Clinical Pathology. — Rheumatic endocarditis is unquestionably 
the most important factor of this variety of valvular disease, which 
ordinarily depends upon an insidious and progressive valvulitis, 
arising, in childhood, in connection with vague arthritic symptoms, 
and being first recognized during the second or third decade of 
life in those who, as young children, suffered from "growing pains" 
and other atypical manifestations of subacute or masked rheumatism. 
Less frequently mitral stenosis is traceable to an acute attack of 
rheumatic fever attended by well-defined endocarditis, and very 
exceptionally the lesion is to be regarded as congenital, being due in 
such instances either to fetal endocarditis or to developmental defect. 
Chorea is also a prominent cause of mitral valvulitis and narrowing, 
and the valvular irritation consequent to anemia and chlorosis, as 
well as the undue stress upon the mitral leaflets imposed by attacks 
of pertussis, may excite fibroid constriction of the mitral orifice. 
Pure mitral stenosis is a disease of children and young adults, rather 
than of advanced life, and is much commoner in females than in males, 
the former fact being generally attributed to the prevalence of rheu- 
matism in the young, and the latter to the susceptibility of girls 
to rheumatism, chorea, and anemia. Persons of middle or advanced 
age occasionally acquire mitral stenosis of a sclerotic type, under 
which circumstances the lesion is but part of a general arterio- 
sclerosis, and is commonly associated with chronic renal disease, 
gout, or syphilis. Rokitansky's theory that mitral stenosis and 
pulmonary tuberculosis are antagonistic is generally regarded as 
tenable. The view that tuberculosis is an exciting cause of mitral 
obstruction, especially of those types characterized by slow develop- 
ment and progress, is supported by Potain and by Tessier. The 
association of mitral stenosis with cholelithiasis, which occurs in 
about one-fifth of all cases of this type of valvular disease, 
according to Brockbank, has never been satisfactorily explained. 

The structural changes in mitral obstruction implicate mainly the 
valve leaflets, their tendinous and muscular attachments, and the 
basal ring of the orifice (Figs. 172 and 173). Of the valve defects, 
the two most distinctive types are known as Corrigan's "button-hole 
mitral" and the so-called "funnel-shaped stenosis," of which the 
former is the commoner in adults and the latter, in children. In the 
button-hole variety of obstruction the valve segments are fused, re- 
tracted, and greatly thickened, with the result that the mitral orifice is 
converted into a mere narrow slit or a somewhat crescentic perfora- 
tion ; in the funnel-shaped stenosis the leaflets are intimately welded 



452 



PHYSICAL DIAGNOSIS 



together, and, by sclerotic shortening of the chordae tendineae, pulled 
down into the cavity of the left ventricle in the form of a conic structure 
the large orifice of which points toward the auricle. In both these 
forms of obstruction the valve mechanism is further interfered with 
by more or less fibrous constriction of the mitral ring and by con- 
traction and rigidity of the tendinous cords and papillary muscles, 
which, in extreme instances, appear to be attached directly to the 
valve leaflets, so striking is the shrinkage of the thickened cords. 




Fig. 172. — Mitral stenosis (Jefferson Hospital Laboratories). 

In some instances, particularly those of congenital type, stricture 
of the orifice by contraction of the sclerotic and calcified basal ring, 
with little or no deformity of the leaflets, is the conspicuous change. 
In other cases the orifice is obstructed by vegetations situated upon 
the auricular surfaces of the leaflets just back of their free borders; 
the constriction may be due to irregular deformities of the cusps, 
depending upon fibrous contraction and the deposit of lime-salts; or, 
rarely, a calcareous plate projects from the basal ring into the lumen 
of the orifice. Ewart mentions pedunculated thrombus attached to 
the left auricular wall as a cause of mitral obstruction, and he has 
also described a narrowing of the mitral orifice due to yielding non- 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



453 



indurative fibiosis, in which type of so-called " soft- valve stenosis " 
a murmur may never develop, owing, Ewart maintains, to the re- 
markable pliability of the valve mechanism. 

A condition of relative mitral stenosis is said to exist when dilatation 
of the left ventricle is associated with no deviation from the normal 
diameter of the auriculoventricular orifice. As a rule, left ventricular 
distention causes corresponding dilatation of the mitral ring, and 
hence relative mitral incompetence ensues, but should the ring fail 




Stenotic mitral 
orifice 



Fig. 173. — Mitral stenosis (Jefferson Hospital Laboratories). 

ro stretch, the orifice necessarily must be stenosed relatively to the 
inordinately large ventricular chamber beyond. 

The immediate effects of mitral stenosis are felt by the left auricle, 
whose walls hypertrophy to a degree proportionate to the increased 
force the auricle must exert to drive the blood through the narrowed 
outlet into the ventricle. This primary auricular hypertrophy may 
ensure a satisfactory blood-supply to the left ventricle for a time, but 
usually not for a long period, as the auricle, having but indifferent 
muscular power, tends soon to dilate under the undue stress, in 



454 PHYSICAL DIAGNOSIS 

some instances enlarging to a most extraordinary degree — even to 
twice or thrice its normal capacity. In fully 50 per cent, of mitral 
stenoses the advanced myocardial degeneration attendant thereto 
ultimately causes auricular fibrillation, in which these chambers 
are maintained in wide diastole with their musculature incessantly 
quivering with fine fibrillary twitching movements, due to the in- 
dependent origin of new impulses in many small areas, but never 
actually contracting through stimuli sent from the sino-auricular 
node (v. s.). Osier has shown that the dilated auricle may 
compress the left recurrent laryngeal nerve, exciting a group 
of pressure symptoms like those attending thoracic aneurism. 
(See p. 501.) It is possible also that the pressure may be exerted 
by the pulmonary artery, or by a mass of mediastinopericardial ad- 
hesions, and that the nerve may be stretched by the drag upon the 
aortic arch and ligament consequent to the coexisting right-sided 
enlargement of the heart. The primary hypertrophy and secondary 
dilatation of the left auricle in mitral stenosis stand in strong con- 
trast to the primary dilatation and secondary hypertrophy 
of this chamber in mitral regurgitation. When the left auricle 
fails, the pulmonary congestion consecutive thereto augments the 
work of the right ventricle, and this chamber now hypertrophies 
and then dilates, in its effort to overcome the stasis of the lesser blood 
circuit. This is unquestionably beneficial, in that the force of the 
hypertrophied ventricle is transmitted through the pulmonary 
circulation into the left auricle, raising the pressure therein, and 
thus aiding the feeble auricular contractions to drive the blood 
column onward through the stenosed mitral orifice. When finally 
the right ventricle fails, relative incompetence of the tricuspid valve 
is inevitable, and ultimately the right auricle, after a period of com- 
pensatory hypertrophy, dilates, with the disastrous consequences refer- 
able to general venous congestion. (Seep. 444.) In pure compensated 
mitral stenosis the left ventricle, having less work than normal to 
perform, not only does not enlarge, but ordinarily diminishes in size, 
becoming atrophied, thin walled, and flabby, and appearing dwarfed 
in comparison with the decidedly hypertrophied right ventricle. Left 
ventricular atrophy, then, is the familiar autopsy finding in uncom- 
plicated mitral stenosis, notwithstanding the contention of some 
authors that the wall of the ventricle overdevelops in consequence 
of its undue efforts in performing diastolic aspiration of the auricular 
blood, with which act an obstructed mitral orifice interferes. When, 
however, compensation breaks and venous stasis is persistent and 
excessive, systemic arterial hypertension is thereby set up, and to 
overcome this resistance the left ventricle commensurately hyper- 






DISEASES OF THE CARDIOVASCULAR SYSTEM 455 

trophies. It also does so, irrespective of broken compensation, in 
that class of cases in which persistent high tension accompanies the 
mitral defect. (Seep. 421.) Left ventricular hypertrophy naturally 
attends double mitral lesions, as the result of the regurgitation. 

Physical Signs. — Inspection. — Interference with the pulmonary 
circulation accounts for the chief objective evidences of mitral stenosis 
— early, persistent, and increasing dyspnea; cough productive of 
liquid, and frequently hemorrhagic, sputum; and cyanosis varying 
in degree from a slight dusky flush upon the cheeks to intense diffuse 
blueness of the face and extremities. Striking pallor of the skin 
and blanching of the mucous membranes, with other evidences of 
well-marked anemia and its consequences, are frequently seen in 
women who suffer from mitral stenosis. As a rule, edema is not so 
conspicuous as it is in mitral regurgitation, though it occurs, of 
course, when right heart failure leads to general venous stasis. 
Clubbing of the finger-tips, and, in children, unnatural promi- 
nence of the lower sternal area, are familiar signs in cases of long 
standing. 

Systolic throbbing is visible in the epigastrium and lower part of the 
sternum when the right ventricle is considerably hypertrophied, and 
the impact of this chamber's conus arteriosus is occasionally percep- 
tible, in thin-chested subjects, at the left of the sternum in the fourth, 
the third, or, rarely, the second interspace. Systolic jugular pulsation 
is noticeable when secondary tricuspid leakage is well established. 
The apex-beat, if strong enough to be seen, is found to occupy an 
approximately normal position. 

Palpation. — In well-compensated mitral obstruction palpation at 
or just above the apex detects, with great constancy, a rough pre- 
systolic thrill occupying either the latter part or the whole of the 
diastolic period, and terminating in a short, sharp ventricular shock. 
Sometimes the thrill is not unlike the soft purring of a cat — hence the 
term, "fremissement cataire" of the French school; and, as a rule, 
it is circumscribed to the neighborhood of the apex, and is intensified 
during expiration, by active exercise, and by left lateral decubitus. 
The discovery of this dual sign — presystolic thrill and systolio 
shock — is of itself proof positive of mitral stenosis. Other tactile 
signs to be noted in this lesion include a sharp impact in the pulmonio 
area, caused by the sudden closure of the pulmonic valve, and also 
the right ventricular pulsations alluded to above. 

Preceding the stage of cardiac breakdown the pulse, though small, 
is of relatively high tension, and regular in rhythm and in frequency, 
the artery being of small size and full between beats, probably in 
consequence of contraction of the general arterial system to ensure 



45^ PHYSICAL DIAGNOSIS 

its accommodation to the diminished ventricular output of blood. A 
radial tracing made at this period indicates a wave of small amplitude, 
characterized by an oblique upstroke, a blunt apex, and a gradually 
falling downstroke having a poorly defined dicrotic notch; later the 
sphygmogram shows most graphically the character of the various 
irregularities of rate, rhythm, and force noticed by feeling the pulse 
during the stage of disturbed compensation. These tracings, how- 
ever, show nothing distinctive. 

Percussion. — Owing to the right ventricular enlargement, the area 
of cardiac dulness extends considerably beyond the right sternal 
border, dulling Ebstein's angle and obliterating the pulmonary 
resonance for a considerable distance to the right of this point, 
between the third and the fifth interspaces. To the left of the 
sternum there may be dulness, generally within the midclavicular 
line, extending from the second or third rib to the apex, the greater 
part of this area corresponding to the site of the enlarged right 
ventricle. In mitral stenosis, with no hypertrophy of the left 
ventricle, the lower left cardiac limit is not unnaturally extended. 
According to Potain, the abnormally large left auricle of a pure mitral 
obstruction is capable of producing an oblong area of impaired 
resonance, about 4 J by 2 £ inches (11.2 by 6.2 cm.) in extent, in 
the left interscapular region, and to the stabbing sensation provoked 
by strong percussion over this area Vasquez has given the name 
" auricular pain." Enlargement of the hepatic area supervenes in 
the late stages of mitral stenosis, in consequence of passive venous 
congestion of the liver. 

Auscultation. — The auscultatory findings in mitral stenosis differ 
very radically according to the mechanical conditions prevailing 
during the progress of the lesion, in view of which Sir William H. 
Broadbent's plan of grouping the sounds and murmurs in three 
stages is most helpful (Fig. 1 74) . In the first stage, that of ade- 
quate compensation, auscultation at the apex affords three dis- 
tinctive sounds: a rough, rumbling presystolic murmur, abruptly 
terminating in a sharp, snappy first sound, 1 and followed, after a 
prolonged diastolic interval, by a distinct, occasionally reduplicated, 
second sound. 2 Rarely, a short interval separates the murmur 

1 The apical first sound may be reduplicated (from asynchronous mitral and 
tricuspid valve closure), but this peculiarity is of far less diagnostic moment 
than the sharp snappiness of the sound. 

2 This reduplication of the second sound at the apex (Sansom's "double shock 
sound") is attributed to sudden tension of the mitral cusps, primarily dependent 
upon increased intra-auricular pressure, whereby the blood-column is driven 
with undue velocity into the ventricle. Apical reduplication of the second 
sound, since it may precede the development of the presystolic murmur, is an 
important early sign of mitral obstruction. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



457 



from the first sound, a peculiarity which Mackenzie attributes 
to delay in the transmission of the contraction stimulus between 
auricle and ventricle. At the base the pulmonic second sound 
is sharply accentuated and frequently doubled, while the aortic 
second sound either remains of normal intensity or is enfeebled. 
The murmur occupies a short interval immediately before ventric- 
ular systole, and is distinguished by rolling, vibratory quality, by low 
pitch, and by gradually increasing intensity, or ingravescence, toward 
its abrupt termination. Its punctum maximum is just above and 




First stage 




KV 






\ Second stage 
i 



AW 



< 



Wtt 



j Third stage 



I II 

Sound Sound 



Murmur 
Fig. 174. — The murmur of mitral stenosis. 



somewhat within the apex-beat, where, as a rule, the murmur is 
sharply localized, though in some instances its audibility extends, 
in the shape of a roughly pyramidal area, from midsternum to mid- 
axilla (Fig. 1 53) . A mitral stenotic murmur, however, is never trans- 
mitted, in the ordinary sense of the word. Although generally 
ascribed to blood eddies created by the auricular contraction, there 
is also truth in Colbeck's belief that the bruit of mitral stenosis like- 
wise may be due to vibrations excited in the long anterior mitral flap 
by the impact of the auricular blood stream. 






45 8 PHYSICAL DIAGNOSIS 

Inconstancy and variation in intensity and duration are other 
peculiarities of this murmur, which is prone to appear and to dis- 
appear erratically in the same patient, and to become soft and in- 
distinct and prolonged when the heart is beating rapidly. The sharp 
snappiness of the apical first sound corresponds to the systolic shock 
felt at the apex, and though both phenomena are obviously due to 
a common cause, their precise nature is a matter of much contro- 
versy; perhaps the best explanation assumes an incomplete filling of 
the left ventricle, whereby the contraction of the muscular wall, at 
first unopposed, is suddenly arrested by contact with the contained 
blood before the completion of systole. 

The second stage, characterized by beginning failure of the left 
auricle and by hypertension of the pulmonary circuit, is accompanied 
by certain alterations in the character of the murmur, by increased 
intensity of the first sound, and by disappearance of the second 
sound at the apex. The murmur, hitherto a short continuous 
crescendo just before systole, now tends to become prolonged and 
wavy or actually interrupted. In other words, it now corresponds 
not only to the time of the auricular systole, but also to the time of 
the ventricular diastole, which creates a suction force at the mitral 
orifice sufficient to generate an additional sound during the early 
part of the diastolic period. It is this suction murmur, due to the 
diastolic recoil of the left ventricle, that accounts for the sound now 
audible at the beginning of diastole, before the appearance of the 
strictly presystolic bruit produced by the auricular force. The 
murmur audible at this stage may occupy the entire diastolic period, 
beginning immediately after the second sound and continuing up to 
the sharp first sound, as a continuous bruit having: (a) a mid-diastolic 
diminuendo and a presystolic crescendo; or (b) a double crescendo 
wave; or (c) a mid-diastolic crescendo and a presystolic diminuendo. 
Should the ventricular suction-action be expended before the auric- 
ular contraction-force begins, the murmur will be actually inter- 
rupted at about the middle of diastole, so that it consists of two 
separate phases — one audible immediately after diastole and the 
other immediately before systole. Should the auricular force fail, 
but the ventricular suction persist, the strictly presystolic rumble 
will be suppressed, in which case but a single short sound, at the 
very beginning of the diastolic period, is detected. Should the 
pressure within the ventricle fall below that within the auricle, the 
characteristic presystolic rumble is replaced by a much softer 
diastolic diminuendo murmur generated at the narrow mitral 
orifice at the moment its valves open. In the event of auricular 
fibrillation, with the abolition of every vestige of the auricular 









DISEASES OF THE CARDIOVASCULAR SYSTEM 459 

contraction force, this diastolic murmur is commonly followed by 
a distinct period of silence just before systole, the adventitious 
sound being ascribed to the increased velocity of the blood flow 
during early diastole and the succeeding silence to the slow- 
ing of the current during late diastole. In general, Dagnini's 
statement is true, that early and mid-diastolic murmurs are 
more frequent in double mitral lesions than in pure stenosis. 
Aside from the changes in the murmur, the increased loudness and 
sharpness of the apical first sound and the disappearance of the 
second sound at the apex are clinically important signs. Maintain- 
ing that the second sound audible at the apex is the transmitted 
aortic (not pulmonic) tone, its disappearance in mitral stenosis is 
commonly attributed to two factors: first, weakening of the aortic 
second sound by the diminished tension of the aortic cusps consequent 
to the restricted output of blood by the left ventricle; and, second, 
non-transmission of this enfeebled aortic second sound to the pre- 
cordia, owing to the backward displacement of the left ventricle by 
the hypertrophied and dilated right heart. Corresponding enfeeble- 
ment of the second sound in the aortic area, and accentuation, 
generally also reduplication, of the second sound in the pulmonic 
area are corroborative of the foregoing explanation. 

The third stage is distinguished by striking enfeeblement or even 
total disappearance of the presystolic murmur, and when this 
happens, the short, sharp first sound is the sole auscultatory 
sign distinguishable at the apex, since already the apical second 
sound has been effaced. Coincidentally, the accentuation of 
the pulmonic second sound at the base disappears, and its aortic 
equivalent becomes still weaker. This stage of the lesion corre- 
sponds to extreme dilatation of the left auricle and the right ven- 
tricle, and to auricular fibrillation, with the establishment of tricus- 
pid leakage and, in consequence, lowering of the pressure within the 
pulmonary circuit and the left auricle. The force of the auricular 
contractions is now so lessened and the tension within the auricle is 
at so low an ebb that a murmur is no longer generated. However, 
should the heart regain its tone, as is not infrequently the case, the 
murmur may reappear, its persistence depending upon the mechanical 
forces active at different periods. In addition to the presystolic 
murmur, the majority of mitral stenoses also afford the systolic bruit 
of mitral regurgitation, and, during the advanced stage, a similar 
sound referable to secondary tricuspid leakage. Sometimes it is 
also possible to recognize the so-called "murmur of high pressure,' 7 
indicative of relative pulmonary leakage. (See Relative Pulmonary 
Regurgitation, p. 485.) 



460 PHYSICAL DIAGNOSIS 

Diagnosis. — A rough presystolic murmur and thrill, with a snappy- 
first sound and a reduplicated second sound at the apex, are character- 
istic of mitral stenosis. Restriction of the murmur and thrill to the 
apical region and their ingravescent quality, accentuation of the pul- 
monic second sound at the base, enlargement of the right ventricle 
rather than of the left, and a small thready pulse are corroborative evi- 
dence not to be overlooked. Later, as the murmur and the second 
sound become indistinct and evanescent at the apex, the character of 
the other heart-sounds are the most definite guides. As the power of 
the heart wanes, the pulmonic second sound, for a long period accen- 
tuated, finally weakens at the base; and the aortic second sound, 
already lost at the apex, becomes almost inaudible in the aortic area; 
but despite all this, the first sound still snaps sharply at the apex. 
This sign, interpreted in the light of other clinical information, may 
be sufficient to warrant a diagnosis of mitral obstruction during the 
stage of broken compensation. 

Discrimination between the Flint murmur of aortic regurgitation 
and the bruit of organic mitral constriction must sometimes be equivo- 
cal, for both are similarly timed, have a common punctum maximum, 
are restricted to the apex, and may be accompanied by the same 
sort of thrill. In a given case of Corrigan's disease with a basic 
diastolic and an apical presystolic murmur, the latter probably 
represents a spurious obstruction, if unattended by a systolic shock, 
a snappy first sound, an accentuated pulmonic second sound, and 
enlargement of the right ventricle. Moreover, a Flint murmur 
generally is less intense, rumbling, and ingravescent than the bruit 
of true stenosis, while the pulse does not become small and thready, 
but retains its collapsing character. Syllaba advises, in studying 
doubtful cases, the use of digitalis, the action of which quiets or 
dissipates the murmur of Flint. 

Tricuspid stenosis, though almost unique as an isolated lesion, 
must not be overlooked as a possible counterfeit of mitral obstruction, 
for a circumscribed presystolic thrill and murmur, with a sharp 
first sound, are common to both. These signs, restricted to the 
tricuspid area and attended by right auricular dilatation and venous 
congestion without pulmonary engorgement, warrant the diagnosis 
of tricuspid obstruction. In doubtful cases it is helpful to remember 
that in this affection, owing to the relatively weak contractions of the 
right auricle, the murmur is likely to be lower and less rumbling, 
while the tactile vibrations are less distinct than in its mitral counter- 
part; and also that, exceptionally, the liver shows presystolic (auricu- 
lar) pulsation. When mitral and tricuspid stenosis coexist the signs 
of the former usually so completely overshadow those of the latter 



DISEASES OF THE CARDIOVASCULAR SYSTEM 46 1 

that the right-sided defect escapes attention. When the tricuspid 
signs are well defined, one sometimes detects two thrills and two 
murmurs of virtually identical nature, save, perhaps, for differences 
in quality and pitch, and for the important fact that one is localized 
at the cardiac apex and the other at the base of the ensiform, 
between which puncta maxima lies a silent area over which neither 
bruit can be heard. Cyanosis, dropsy, and other evidences of 
venous obstruction are no criteria in distinguishing right- and 
left-sided auriculoventricular stenoses, nor is the character of the 
pulse a guide. 

Pericarditis in children is occasionally followed by the development 
of a rumbling presystolic apical murmur, which Broadbent believes 
is " possibly a result of pericardial adhesions." This murmur, 
unlike that of true mitral stenosis, lacks a vibratory, crescendo 
character, and does not terminate abruptly in a snappy first sound; 
while the exocardial origin of such a bruit is suggested by its appear- 
ance after an attack of pericarditis and by its association with other 
physical signs thereof. 

In those affected with the effort syndrome (q. v., p. 403) and suffer- 
ing from various infectious diseases a presystolic apical thrill, with 
reduplication of the first sound and a perceptible systolic shock, is 
frequently appreciable. This syndrome, which is not associated 
with evidences of organic cardiac disease, is exaggerated by phys- 
ical exercise and by emotional influences, and does not, under such 
circumstances, "disqualify for full, active military service" (Morris; 
Friedlander) . 

AORTIC REGURGITATION 

Clinical Pathology. — This dangerous type of heart disease was 
first established as a clinical entity in 1832 by the brilliant Irish 
physician, Sir Dominick Corrigan, who termed the lesion a "perma- 
nent patency of the mouth of the aorta." Ordinarily, it affects 
men of middle age, and is the consequence of a gradual, progressive 
sclerosis, of which unremitting muscular strain, alcohol, and syphi- 
lis, combined or singly, are the material factors ; to some degree it 
is probable that plumbism and gout have a similar influence. The 
essential cause, then, of this type of heart disease consists of long- 
continued irritation of the aortic cusps, both by their exposure to 
excessive tension during diastole and by the action of circulatory 
poisons: This being so, it is easy to understand the predilec- 
tion of aortic leakage for sailors, soldiers, stevedores, stokers, and 
other men whose occupations entail habitual muscular strain and 



462 



PHYSICAL DIAGNOSIS 



whose tastes perchance run to alcohol and to venery. " Athlete's 
heart" and "jinrikisha heart" are medical slang for the aortic 
regurgitation occurring in the athlete, and in the rickshaw man of the 
Orient. Less commonly the aortic leaflets are damaged by endocar- 
ditis, whereby valvular induration, puckering, and adhesion, together 
with vegetation, erosion, and dense fibrocalcareous deformity, are the 




Wall 



Aortic orifice 

Fig. 175. — Aortic regurgitation and double mitral lesion. Aortic and auricular 
aspects (Jefferson Hospital Laboratories). 



various lesions provoked, according to the extent and malignancy of 
the inflammation. In regurgitation of endocarditic origin it is also 
true that males are more predisposed than females, but here middle 
age is not a prominent etiologic factor. Traumatic aortic regurgita- 
tion, from rupture of a leaflet, though very rare, occasionally follows 
a sudden violent strain; it is hard to believe that this accident can 
happen so long as the valve is normally resistant, though when 
damaged by sclerosis or erosion, a cusp is not unlikely to be torn or 
perforated under the stress of great muscular exertion or even by 



DISEASES OF THE CARDIOVASCULAR SYSTEM 463 

inordinate arterial hypertension. Exceptionally, the aortic orifice 
leaks because the valve is congeni tally malformed, and in such 
instances it is usual to find sclerotic valvulitis with fusion of two cusp 
borders, and hence, conversion of the valvular apparatus into a double 
instead of a triple set of leaflets. Aortic regurgitation, whether 
sclerotic or endocarditic, is commonly attended by more or less 
stenosis, owing to the frequent coincidence of fibrous contraction 
at the aortic ring sufficient to obstruct the systemic blood-column 
passing through this aperture. The systemic arteries do not often 
escape fibrosis, owing to the circulatory wear and tear provoked 
by the powerful ventricular contractions, which, despite their force, 
are not always able properly to fill the arteries, if the aortic reflux 
be excessive. The circulation within the coronary arteries is greatly 
disturbed, and these vessels are damaged by sclerotic degeneration — 
defects leading to muscular degeneration of the heart. In many 
instances the first part of the aorta is the seat of fibrosis, atheroma, 
and calcification, whereby permanent dilatation is favored. So-called 
" dynamic dilatation" of the aortic arch, simulating the physical 
signs of aneurism and occasionally met with in Corrigan's dis- 
ease, is due merely to the violent systolic shocks of the voluminous 
blood-columns within a resilient and distensible aorta, having no 
actual enlargement of its caliber and no traces of mural disease. 

Aside from the foregoing types of aortic reflux, essentially referable 
to valvular deformity, regurgitation also occurs into the ventricle 
when the aortic ring and the ventricular wall are so stretched that the 
leaflets of the valve fail to approximate during diastole. This 
so-called relative aortic incompetence is much less common than a 
corresponding leakage at the mitral orifice, since the aortic ring, 
being stouter and denser, does not readily enlarge to a caliber render- 
ing perfect coaptation of its valve cusps impossible. Relative aortic 
incompetence follows stretching of the aortic ring secondary to 
myocardial degeneration, atheromatous dilatation of the aortic root, 
aneurism of the ascending arch of the aorta, and pressure stenosis 
of this vessel. 

In aortic regurgitation the left ventricle bears the brunt of the 
damage, since with diastole this chamber receives not only its normal 
quota of blood from the auricle, but also the stream regurgitated 
from the aorta through the leaky semilunar cusps. Surcharged in 
this manner, the ventricle dilates in order to accommodate the undue 
blood volume, and hypertrophies so as adequately to propel its 
contents aortaward. This habitual overwork in time creates that 
extreme grade of eccentric hypertrophy of the left ventricle termed 



464 



PHYSICAL DIAGNOSIS 



cor bovinum, or ox heart, the weight of which may be three or even 
four times that of the normal organ (Fig. 1 64). So long as this conserv- 
ative hypertrophy predominates, the valvular lesion is compensated 
by the increased ventricular output thereby made possible, but inevit- 
ably dilatation gains the upper hand, owing to the pernicious action 
of the persistent ventricular overdistention and to myocardial mal- 
nutrition due to defective coronary blood-supply. When, finally, the 
ventricle gives way and no longer can pump sufficient blood into the 
systemic circuit to satisfy its demands, failure of compensation super- 
venes. Relative leakage at the auriculo ventricular orifice occurs with 
systole, because of the strain upon the mitral ring, if, indeed, the 
valve's integrity is not already impaired by pathologic changes, and 
in consequence of this incompetence a wave of backward pressure is 
transmitted into the left auricle, the pulmonary veins, and the right 



Aortt 




Mtral 



-Cor 
bovinum 



Diastole 
Fig. 176. — Mechanism of the murmur of aortic regurgitation. 

heart, with the baneful effects already recounted in connection with 
mitral regurgitation. (See p. 447.) 

Physical Signs. — Inspection. — Violent arterial throbbing is a 
noteworthy sign of Corrigan's disease, and in some instances one is 
almost justified in hazarding the diagnosis by this evidence alone. 
The pulsations, systolic in time and perhaps so vigorous as to jog the 
patient's head with every heart-beat (Musset's sign) , are particularly 
conspicuous in the carotid and subclavian arteries of the neck, in 
the temporals of the face, and in the brachials of the arm, while in 
the episternal notch an aortic throb is generally visible. Even the 
small arteries, such as the radial and the dorsalis pedis, may pulsate 
visibly, showing in miniature the powerful beats of the larger arterial 
trunks. If tortuous, a superficial artery, such as the brachial, may 
not only pulsate, but even become displaced and elongated with 
every beat — the locomotive or movable pulse. Penetration of the 



DISEASES OF THE CARDIOVASCULAR SYSTEM 465 

capillaries by the pulse-wave produces pulsation of these small 
vessels, to which the term capillary pulse is applied (see p. 353); 
and, rarely, the superficial veins, notably those of the hand and 
forearm, show postsystolic undulations created by arterial waves 
of sufficient force to penetrate the delicate venous radicles — the 
penetrating, direct, or centripetal venous pulse. (Seep. 357.) Pulsa- 
tion and tortuosity of the retinal arteries are sometimes visible with 
the ophthalmoscope. The precordial area heaves under the impact 
of the enlarged heart, and, in the case of a thin-walled, resilient 
thorax, it may show unnatural protrusion. A violent pulse in the 
abdominal aorta causes an epigastric throb. The apical impulse 
appears extraordinarily broad and powerful, and is displaced from 
one to three interspaces downward and outward toward, if not, 
indeed, as far as, the left anterior axillary line. In certain subjects 
atmospheric pressure produces a circumscribed systolic recession of the 
third and fourth interspaces between the left sternal and midclavicular 
lines, and in such instances a systolic thrill at the apex may be very 
closely counterfeited by costal vibrations set up by the violent and 
sharp cardiac impulse. These remarks apply to a well-developed 
example of aortic regurgitation with decided left ventricular hyper- 
trophy, considerable reflux from the aorta, and marked arterial 
relaxation, but when such conditions do not obtain, it is obvious that 
suitable modifications of these visual signs are to be made. Pallor 
of the skin and mucous membranes is a common sign in aortic 
regurgitation, especially during the advanced stages, and, when 
compensation fails, cyanosis, dyspnea, cough, edema, and other 
evidences of venous obstruction supervene. Ague-like attacks not 
infrequently light up from time to time as a symptom of recurrent 
endocardial inflammation. 

Palpation. — A heaving, tumultuous, lifting impulse of wide extent 
i:, perceived by laying the palm of the hand upon the precordia, but 
later, as dilatation predominates, this sign of ventricular hypertrophy 
is replaced by a feebler, less extensive, and somewhat undulatory 
pulsation. Occasionally there is a prolonged diastolic thrill at 
the base of the heart, due to vibrations excited by the regurgitant 
blood-column; a systolic thrill in the episternal notch, if the aorta 
be greatly dilated; and a presystolic thrill near the apex, suggestive 
either of a Flint murmur or of a true mitral stenosis (v.i.). Rarely 
a distinct thrill may be felt over one of the smaller arteries, such as 
the brachial. A short, sharp diastolic impact in the region of the 
apex suggests sudden recoil of the left ventricle under the burden of a 
large volume of reflux blood. Rarely, it is possible to distinguish 



466 PHYSICAL DIAGNOSIS 

arterial pulsation over the liver, and, very exceptionally, over the 
spleen. One obtains a good idea of the general arterial over- 
action by grasping, with firm compression, the subject's arm just 
above the elbow, so as to obstruct the circulation and create 
an exaggerated distensive pulsation proximal to the constriction 
(Hawke). 

Gordon notes that in young subjects the diastolic murmur of a 
slight aortic leakage may completely disappear when a deep breath 
is taken and held, explaining this peculiarity by the neutralized 
elastic recoil and diminished fulness of the aorta due to the thoracic 
negative pressure excited by a forced inspiratory effort. 

The pulse is very characteristic in most cases of aortic regurgitation; 
it is commonly known as the "Corrigan pulse," owing to its lucid 
description by Corrigan, but is also termed the "pulsus altus et celer," 
the " pulsus celerrimus," the "water-hammer pulse," the " collapsing 
pulse," the "receding pulse," and the "pistol pulse." In the radial 
arteries the pulse-wave rises suddenly and with extraordinary force, 
strikes the palpating finger with a momentary shot-like impact, and 
then instantly collapses, the strong impact representing the concussion 
of the large column of blood hurled aorta ward by the hypertrophied 
left ventricle, and the quick collapse indicating the rapid depletion 
of the arteries due to diastolic reflux of the blood-column through 
the leaky aortic valve into the left ventricle. The Corrigan pulse, 
particularly its collapsing character, is exaggerated by raising the 
subject's arm vertically above the head, so as to take advantage of 
the force of gravity; its peculiarities are masked by arterial sclerosis 
of a grade sufficient to impair the resiliency of the vessels and hence 
their ability to carry an undue volume of blood. Dilatation of the 
left ventricle with mitral insufficiency also negatives this pulse, by 
weakening the ventricular systole and diminishing the output of 
blood. As the cardiac strength wanes the pulse quickens, weakens, 
and becomes irregular in time and in force, and occasional extra 
systoles of a tired ventricle become perceptible between the more 
forcible beats. An unduly long interval between the apical impulse 
and the radial beat indicates a prolonged ventricular systole. 

The characteristic pulse tracing of aortic leakage indicates great 
amplitude, showing a high, abrupt upstroke, a sharp apex with an 
acute angle, and a rapidly falling downstroke, having a poorly de- 
fined, if not entirely obliterated, dicrotic undulation. (See Fig. 130, 
xiii ; p. 349.) The exaggerated amplitude and the sudden rise and 
fall of the tracing, so distinctive of this sphygmogram, are materially 



DISEASES OF THE CARDIOVASCULAR SYSTEM 467 

modified by myocardial failure, by concomitant mitral incompetence, 
and by arteriosclerosis. 

Recent experimental studies by H. A. Stewart indicate that aortic 
leakage is accompanied by a fall of systolic blood-pressure presum- 
ably due to increased capillary flow. Leonard Hill has proved that 
the systolic blood-pressure of the leg greatly exceeds that of the 
arm, a difference of from 50 to 100 mm. of Hg being not unusual, 
whereas in health this difference is seldom greater than 10 mm. 
Unduly low diastolic pressures with high pulse-pressures are the 
rule in the average case. 

The palpatory method of sphygmomanometry is usually pre- 
ferred to the auscultatory in aortic regurgitation, owing to the 
persistence of a murmurish tone during the phases ordinarily occu- 
pied by the sharp and dull sounds preceding and coinciding with 
the diastolic pressure stage. But, despite this confusing element 
of sound, it is rarely impossible to identify the dull tone of the 
minimal pressure. (See p. 33.) 

Percussion. — There is downward and outward extension of the 
cardiac area, commensurate with the displacement of the apex-beat 
already noted, and, after compensation breaks, this area perceptibly 
broadens, the left limit of the dilated left ventricle extending upward 
and outward and its apical outline becoming blunt. Ultimately, 
the cardiac dulness may encroach well beyond the right sternal 
border, as secondary enlargement of the right ventricle progresses. 

Auscultation. — During ventricular diastole a murmur is audible 
at the base of the heart whence it is transmitted, with variable dis- 
tinctness, downward over the precordia, and, exceptionally, beyond 
this limit (Fig. 156). The murmur is peculiar in having no constant 
punctum maximum and no definite line of propagation common to 
every case, these two details of the sound varying with the nature of 
the structural changes predominating in the individual heart. 
The murmur usually is louder and more distinct at about the middle 
of the sternum at the level of the third rib rathe*- than at the tradi- 
tional aortic cartilage, or it may be heard most clearly along the left 
sternal border at some point between the third rib and the ensiform, 
while exceptionally the punctum maximum is at the apex. A sort of 
double punctum maximum is sometimes definable: one at the apex 
and the other at the aortic cartilage, between which two points the 
bruit is either quite inaudible or greatly suppressed. 

The murmur may be propagated along one of three different lines, 
vertically downward along the sternum to the ensiform cartilage, 
obliquely downward toward the apex, or horizontally outward toward 



468 



PHYSICAL DIAGNOSIS 



the left axilla; occasionally an attenuated diastolic bruit is audible 
over the subclavian and the carotid arteries. The murmur begins 
with diastole, and its greatest intensity coincides with the second 
sound, after which it is prolonged, as a gradual diminuendo, 
generally throughout the entire diastolic period, but occasionally 
subsiding before its completion. The quality of the sound is more 
often soft and blowing than loud and rasping, and its pitch is 
tolerably high; rarely, it is distinguished by an unmistakably musical 
tone, in which event considerable valve laceration is suggested. The 
murmur may be so faint as to be almost inaudible — indeed, extensive 
leakage at the aortic orifice sometimes exists with no murmur at 
all — and its intensity is no criterion of the extent of the endocardial 
damage. 
The aortic second sound is partly or wholly replaced by the murmur, 



Aortic\ 




Fig. 177. — Mechanism of the Flint murmur of aortic regurgitation. 

persistence of the second sound probably meaning a less serious 
aortic leakage than total masking of the tone by the murmur. 
In judging the intensity of the aortic second sound one should always 
auscultate over the carotid artery, in order to eliminate the pulmonic 
second sound, inaudible in this situation. The first sound at the 
base may be distinct and clear and loud, but more often it is obscured 
by a systolic bruit attributable to several causes — roughening of the 
aortic leaflets, atheroma or dilatation of the aorta, true stenosis of the 
aortic orifice, or anemia. The addition of this systolic sound pro- 
duces the familiar "see-saw" or "to-and-fro" murmur of a double 
aortic lesion. At the apex the first sound is likely to be muffled, 
or perhaps overshadowed by the bruit of mitral leakage, either 
relative or organic. The apical second sound is unduly feeble, and 
not uncommonly tinctured with the diastolic bruit reflected thence 
from the base. The rough presystolic murmur of Flint (see p. 390) 
is also audible at the apex in a certain proportion of cases — in 
about 50 per cent., says Thayer (Fig. 177). In certain instances 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



469 



auscultation over the femoral artery reveals a sudden systolic thud 
coincident with the abrupt distention of the arterial wall by the 
impact of the blood-column, which sound, appreciable only when 
very gentle stethoscopic pressure is used, gives way to a physiologic 
constriction murmur when the pressure is increased. Duroziez's 
sign, consisting of this normal systolic bruit plus a diastolic murmur 
of arterial reflux, can often be developed by carefully graduating 
the pressure over the vessel until it is constricted to the exact degree 
essential for the creation of this distinctive double sound. (See 
p. 401.) Exceptionally, auscultation over the femorals reveals a 
faint double sound, not unlike that of the heart-beat — Traube's sign. 

Diagnosis. — Arterial throbbing, a tumultuous apex-beat, col- 
/apsing radial and visible capillary pulses, enlargement of the left 
ventricle, and a diastolic aortic murmur, propagated downward and 
toward the left, unmistakably indicate Corrigan's disease, apart from 
the less constant corroborative signs of this lesion that also may 
be demonstrable. Subjects ot aortic incompetence usually suffer 
from throbbing headache, vertigo, phosphenes, and tinnitus, while 
precordial pain, even true angina, is more common in this lesion 
than in any other type of valvular affection. Aortic disease, espec- 
ially regurgitation, is not infrequently attended by most distressing 
mental symptoms — insomnia, dreadful dreams, melancholia, suicidal 
mania, and delirium. In this connection it may be noted that so- 
called " heart-disease delirium " may be counterfeited by the mental 
symptoms due to the toxic effect of digitalis, as H. O. Hall has 
pointed out. 

The differentiation of aortic regurgitation from pulmonary regurgi- 
tation hinges upon the arterial phenomena and the nature of the 
cardiac structural changes, the details of which are dealt with in 
another place. (See p. 485.) In a preceding section (see pp. 386 
and 399) the characteristics of diastolic anemic and cardiorespiratory 
murmurs sometimes audible at the base of the heart are considered. 

The Flint murmur and the mitral stenotic bruit have been com- 
pared in the diagnosis of mitral stenosis. (See p. 460.) 

AORTIC STENOSIS 

Clinical Pathology. — Stenosis, like insufficiency of the aortic 
orifice, is more frequently attributable to a slow sclerosis than to 
frank endocardial inflammation, and is prone to affect men past 
the prime of life, in whom more or less general arterial fibrosis 
exists. In rare instances the obstructive lesion is the relic of an 
antenatal process. Pure aortic stenosis is the rarest acquired 



47° 



PHYSICAL DIAGNOSIS 



valvular defect of the left heart, for in the vast majority of stenoses 
there is also reflux of blood through the orifice. 



Wall of aorta 
Stenotic orifice of aorta 




'M Atheromatous wall of 
W~ aorta 



Vegetations of surface 
of valve cusp 






Fig. 178. — Aortic stenosis (Jefferson Hospital Laboratories). 

Obstruction to the flow of blood from the left ventricle into the 
aorta ordinarily is due to rigidity and thickening of the semilunar 



;w 




Mitral 



Aorti 



pimple 
tiy]>ertroJ>/iy 



Systole 
Fig. 179. — Mechanism of the murmur of aortic stenosis. 

cusps, whereby they fail closely to hug the aortic wall during sys- 
tole, and hence impede the outflowing blood-stream propelled by 
the ventricular contractions (Fig. 179). In some cases the orifice is 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



471 



obstructed by vegetative excrescences, by simple adhesion of the 
valve borders, or by the formation, by fusion of the cusps, of a 
constricted funnel-like communication between the ventricle and the 
aorta. Calcification of the valve-leaflets, as well as vegetative and 
calcareous changes in the interventricular septum at the attachment 
of the aortic mitral cusp, may also develop. A type of aortic stenosis, 




Fig. 180. — Dilatation of the aortic arch (Jefferson Hospital). 



due not to valvular deformity, but simply to fibrocalcareous con- 
striction of the aortic ring, also has been described. In congenital 
lesions it is the rule to find adhesion and thinning of the aortic cusps 
with little or no evidence of atheroma ; or the defect may be a so- 
called subaortic stenosis, consisting of a constriction of the ventric- 
ular chamber by a ring of endocardial thickening situated below 
the aortic cusps — a process comparable to the conal type of pul- 
monary stenosis (q.v.i.). Occasionally, neither valve nor ring is 



472 PHYSICAL DIAGNOSIS 

affected, but the aorta immediately beyond the latter is dilated — a 
condition known as relative aortic stenosis, though obviously " di- 
latation of the aorta" is the better term for the condition. The 
walls of the aortic arch are very commonly the seat of fibrocalca- 
reous degeneration. 

The immediate effect of aortic obstruction is a gradual and 
progressive thickening of the wall of the left ventricle, primarily 
unattended by dilatation. This change, one of so-called simple 
hypertrophy, is referable to the increased work thrown upon the 
ventricle in its endeavor to force the blood through an unduly narrow 
aortic opening. Later, however, the ventricle tends to give way 
under the incessant strain and to suffer myocardial degeneration, 
due to coronary artery occlusion, and in consequence it dilates, 
perhaps so decidedly that relative mitral leakage ensues, and in 
time the left auricle, the pulmonary circuit, and the right ventricle 
are affected by the back pressure. 

Physical Signs. — Inspection. — The subject of aortic stenosis 
shows little or no evidence of a diseased heart so long as the left 
ventricle does not flag and the mitral valve remains tight, but when 
these structures give way signs of an embarrassed pulmonary circula- 
tion, already described, appear. Anemic pallor is likely to develop 
in the. course of time, and in arteriosclerotic patients exaggerated 
prominence and tortuosity of the hardened surface vessels attract 
attention at first glance. The apical impulse, apparently of fair 
force, is dislocated obliquely downward and somewhat outward; or, 
as in old emphysematous individuals, the apex-beat may be looked 
for in vain. 

Palpation. — With tolerable constancy a rather coarse systolic 
thrill, usually most intense at the aortic cartilage, is felt at the cardiac 
base, and, rarely, over the larger arteries near the surface. The 
apex-beat, if palpable, is regular, slow, deliberate, and heaving until 
the disturbing effects of left ventricular failure come into play. 

The pulse of pure aortic stenosis {pulsus tardus) has a slow rate, 
moderate or small volume, normal rhythm, and prolonged, deliberate 
rise and fall. The tracing of such a pulse is quite distinctive, the 
wave being of diminished height, and composed of an unduly ob- 
lique ascent, a blunt apex, and a gradually falling down-stroke, with 
indistinct secondary oscillations. Or, the tracing may register the 
double apex of a pulsus bisferiens, suggestive of a double-phased 
contraction of the ventricle; while sometimes the notched upstroke 
of anacrotism is shown. (See Fig. 130, ix, x, xiv; p. .349.) 






DISEASES OF THE CARDIOVASCULAR SYSTEM 473 

Percussion. — The downward and outward extension of cardiac 
dulness is proportionate to the degree of left ventricular enlargement, 
but in the average case of aortic stenosis the precordial limits are 
much more restricted than in Corrigan's disease. Impairment of 
pulmonary resonance at the right of the sternum may be detected 
as a late finding should secondary hypertrophy of the right ventricle 
occur. 

Auscultation. — Aortic stenosis is attended by a systolic basic 
murmur having its punctum maximum at the aortic cartilage, whence 
it is transmitted into the carotid arteries, and in some instances over 
the entire precordia; most exceptionally, it is also audible alongside 
the spine, over the course of the descending thoracic aorta. Typically, 
the bruit is loud and rough and rasping; atypically, it is soft and blow- 
ing, or musical. The aortic first sound is likely to be masked by the 
murmur, particularly when this synchronous tone is notably harsh 
and intense. The aortic second sound is more or less muffled and 
enfeebled, sometimes to the point of actual extinction, this highly 
suggestive sign of aortic obstruction depending upon rigidity and 
thickening of the valve-leaflets. As a rule, the aortic second sound 
is still further obscured by a diastolic bruit, owing to the frequency 
of an associated leakage at the aortic orifice. The first sound at the 
apex is dully muscular in quality, and the second sound in this 
situation is indistinct, or perhaps blended with the transmitted 
bruit of a coexisting reflux. 

Diagnosis. — A systolic basic thrill, an aortic systolic murmur 
propagated into the neck, and impairment of the aortic second 
sound together determine the diagnosis of aortic stenosis, of which 
lesion moderate enlargement of the left ventricle and a pulse indicating 
slow, deliberate, and often double-phased ventricular systoles are 
highly corroborative. True aortic stenosis is unusual as an isolated 
defect, whereas aortic systolic murmurs, most often symptomatic 
of atheroma or dilatation of the aortic arch, or of some functional 
inadequacy of the heart, are very common. 

Atheroma of the aorta may precisely simulate aortic stenosis in so 
far as the time, quality, and transmission of the bruit are concerned, 
but in atheroma a thrill is exceptional, suggestive pulse changes are 
lacking, arteriosclerotic hypertrophy of the left ventricle exists, and, 
most important of all, the aortic second sound rings clearly at the 
base of the heart. Well-defined arteriosclerosis is in favor of aortic 
atheroma, though the arteries are hard in many examples of stenosis. 

Dilatation of the aortic arch, whether diffuse or aneurismal, also 
accounts for an aortic systolic murmur which is conducted into the 



474 PHYSICAL DIAGNOSIS 

neck, as well as for a corresponding thrill, in many instances. 
In simple dilatation of the aorta one looks for systolic pul- 
sation and unnatural dulness over the ascending aortic arch, 
throbbing in the suprasternal notch, a pulse of fairly good volume, 
and either accentuation of the aortic second sound or its modification 
by a bruit of concomitant aortic leakage. In differentiating aneurism 
of the aorta, attention should be directed to certain distinctive signs 
of this affection: an area of circumscribed dulness affording systolic 
pulsation and diastolic shock, a loud, low-pitched aortic second 
sound, and pressure symptoms affecting the pulses, the pupils, and 
the voice. The value of these findings as diagnostic criteria is dealt 
with more fully in another place. (See p. 501.) The discrimina- 
tion between aortic stenosis and mitral regurgitation, pulmonary 
stenosis, and patent ductus arteriosus is given under these headings. 
(See pp. 451, 482, and 487.) j 

TRICUSPID REGURGITATION 

Clinical Pathology. — Tricuspid regurgitation, due to organic 
valvular lesions or to relative muscular deficiency, is established when, 
during systole of the right ventricle, blood escapes thence through 
an incompetent tricuspid orifice into the right auricle, as well as 
forward into the normal outlet through the pulmonary artery. 
Organic tricuspid regurgitation is comparatively uncommon as a 
clinical finding, though it is not improbable, as Bramwell suggests, 
that the tricuspid leaflets are frequently invaded by inflammatory 
processes which abate without permanently crippling the valve 
mechanism, owing to the tendency of such lesions to undergo perfect 
resolution under the low pressure of the lesser blood circuit. The 
organic defects accountable for tricuspid leakage do not differ mater- 
ially, either in origin or in kind, from those productive of mitral 
regurgitation, endocarditis and sclerotic degeneration of the cusps 
and their tendinomuscular attachments being the factors inter- 
fering with the integrity of the valve. Fibrous induration, thick- 
ening, and puckering of the valve segments, shortening of the chordae 
tendineae, and sclerosis of the musculi papillares are familiar patho- 
logic findings; or the free auricular border of the valve may be the 
seat of vegetations indicating endocardial inflammation of the acute 
or chronic benign variety, or of the malignant type; in the latter the 
mural endocardium is also most likely to be similarly implicated. 
Sclerotic degeneration is commoner at the tricuspid orifice than 
active inflammation, — just the reverse of the conditions prevailing at 
the mitral opening, — such changes supervening as the result of per- 



DISEASES OF THE CARDIOVASCULAR SYSTEM 475 

sistent pulmonary hypertension, and consequently being secondary 
to mitral lesions (especially stenotic), left ventricular dilatation, 
arterial sclerosis, and chronic indurative affections of the lungs, all 
of which obstruct the pulmonary current, and by so doing excite 
habitually high tension within the right ventricle. Traumatic 
tricuspid leakage, due either to cusp laceration or to tendinous rupture, 
is most unusual, owing to the natural tendency of the right auriculo- 
ventricular sphincter to stretch and thus permit a "safety-valve" 
regurgitation, under sudden and acute intraventricular stress (v. /.). 

Relative tricuspid regurgitation, consequent to muscular inadequacy, 
is an exceedingly common lesion, consisting essentially of right 
ventricular dilatation, stretching of the tricuspid ring, and relative 
shortening of the chordae tendineas and musculi papillares, as the 
result of which the valve cusps cannot approximate accurately with 
systole, and hence permit reflux into the right auricle at this time. 
So-called " safety-valve regurgitation, " a truly conservative condition, 
occurs at the tricuspid orifice when, as the result of increased pul- 
monary tension and distention of the right ventricle, the tricuspid 
sphincter enlarges so as to permit a backward leakage which relieves 
the stress upon the ventricular wall and lowers the tension of the 
pulmonary circulation. This natural tendency of the tricuspid valve 
automatically to ease the strain upon the right heart is well illustrated 
by the transient tricuspid leakage provoked by violent muscular 
exercise. Relative tricuspid regurgitation may attend true organic 
valvular disease, but it sometimes exists with perfectly healthy valves; 
its persistence is determined by the character of the underlying cause. 
Relative incompetence of the tricuspid valve from muscular deficiency 
of the right ventricle is a common secondary development in fever, 
anemia, toxemia, and other factors of myocardial relaxation, mal- 
nutrition, and degeneration; it accompanies conditions of heightened 
pulmonary tension consecutive to pulmonary fibrosis and emphysema, 
mitral disease, and left ventricular dilatation, and develops in con- 
sequence of pulmonary stenosis. 

Physical Signs. — Inspection. — Free tricuspid leakage attended 
by right auricular dilatation cannot long exist without producing 
unmistakable evidences of an impeded venous circulation, such as 
cyanosis, edema, and distention and pulsation of the visible veins. 
Dyspnea and cough are also common features, either as forerunners 
of the right-sided heart failure, or arising indirectly from this accident, 
by the extension of the back pressure to the lungs through the sys- 
temic capillaries and arteries. The patient's cyanosis varies with 
the inadequacy of blood aeration existing in the individual case; 



476 PHYSICAL DIAGNOSIS 

the edema, commonly beginning as' dropsy of the feet and ankles, 
ultimately tends to implicate the serous sacs in the guise of ascites 
and hydrothorax, the latter being prone to affect the right pleural 
cavity. Turgescence of the small veins of the surface, in some 
instances most conspicuous, is detected by inspection of the upper 
anterior thoracic wall and the extremities. The external jugular 
veins are unnaturally distended, and, when emptied by pressure, 
nil from below; they may show the systolic pulsation of a positive 
venous pulse, the presystolic pulsation of a negative venous pulse, 
or a double jugular pulsation due to the coexistence of both types 
of pulse. (See Venous Pulse, p. 354.) 

Palpation. — There is epigastric pulsation, due to enlargement of 
the right ventricle, and varying in force with the strength of this 
chamber's contractions. Palpation of the liver discovers a positive 
venous pulse over this organ if the reflux venous waves created by 
the ventricular systoles are conducted thereto. The distinctive 
expansile property of this type of pulsation is to be distinguished 
from the mere lifting impulse of a liver jogged by the impact of a 
hypertrophied right ventricle; bimanual palpation, raising the liver 
with one hand and feeling its anterior surface with the other, is the 
most certain method of appreciating these differences. 

The pulse of tricuspid regurgitation is in no wise characteristic, 
such irregularities as may exist being attributable to concomitant 
lesions of the left heart. A relatively feeble radial pulse on the right 
side suggests compression of the right subclavian artery by an 
enlarged right auricle (PopofT). 

Percussion. — Owing to enlargement of the right heart, cardiac 
dulness extends unnaturally beyond the right border of the sternum 
and downward, while more often than not one also finds impairment 
of resonance due to enlargement of the left ventricle. Congestion 
of the liver produces lengthening of the vertical lines of hepatic 
flatness, the edge of the organ often reaching far below the costal 
margin. 

Auscultation. — The murmur of tricuspid incompetence is most 
distinct over the lower part of the sternum, as a soft, blowing, systolic 
sound, which, though not propagated along hard-and-fast lines, is 
audible over a roughly triangular region lying between the tricuspid 
area, the right midaxillary line, and the manubrium (Fig. 158); 
inconstantly the bruit, enfeebled, is also heard in the neighborhood 
of the apex. The punctum maximum of the murmur is commonly 
situated at the conventional tricuspid area, but as the right ventricle 
undergoes changes in size and shape, the point correspondingly 



DISEASES OF THE CARDIOVASCULAR SYSTEM 477 

shifts — to the xiphoid cartilage; to the left sternal edge over the fifth 
or sixth costal cartilages, or to the right sternal edge over the third, 
fourth, or fifth cartilages. The tricuspid first sound is masked by 
the attendant murmur, but only exceptionally is it entirely suppressed. 
In pure tricuspid leakage the pulmonic second sound is enfeebled; 
accentuation and reduplication suggest coexistent left-sided disease. 
Auscultation over a pulsating cervical vein may reveal a systolic venous 
bruit. It is the rule to find at the apex signs of coexisting mitral 
disease to which the right-sided leakage is secondary. 

Diagnosis. — A systolic (ventricular) jugular and hepatic pulse, 
a tricuspid systolic murmur conducted toward the right, enfeeblement 
of the pulmonic second sound, enlargement of the right heart, and 
evidences of venous obstruction are the typical findings of this lesion. 
Moderate tricuspid leakage, so long as the tone of the right auricle 
is adequate, affords none of the foregoing venous phenomena, and 
in such an instance there may be merely a soft systolic whiff, audible 
over the lower part of the sternum. Furthermore, it is probably 
true that tricuspid regurgitation, especially of the muscular or "safety- 
valve" types, not infrequently gives rise to no physical signs whatever. 

TRICUSPID STENOSIS 

Clinical Pathology. — This exceedingly rare lesion may be of 
acquired or of congenital origin, and in either event is almost invaria- 
bly associated with other cardiac damage, examples of pure isolated 
tricuspid stenosis being most unusual. The acquired form, making 
up the great majority of all cases, occurs most commonly during the 
second decade of life in women who give a history of rheumatic 
endocarditis, and who also suffer from mitral stenosis. The mi- 
tral affection, inducing protracted hypertension within the right 
ventricle, and hence irritation of the tricuspid segments, is the 
primary cause of many tricuspid stenoses, though there is good 
reason for believing that sometimes both auriculoventricular valves 
are simultaneously attacked by a wide-spread inflammation. Aside 
from stenosis due to well-defined inflammation of the endocardium, 
the defect occasionally arises in consequence of slow valvular sclerosis. 
In general, the structural changes affecting the tricuspid valve 
mechanism are similar to those of its mitral counterpart, except that 
on the right side of the heart the degree of constriction is likely to be 
less advanced, probably because the mitral lesion is usually primary 
and, therefore, older than the tricuspid defect, and, unlike the latter, 
tends to persist and to progress, rather than to undergo resolution. 



478 



PHYSICAL DIAGNOSIS 



Congenital tricuspid stenosis, the product of fetal endocarditis or of 
developmental anomaly, is less common than the acquired type. 
It is almost invariably attended by other defects of cardiac develop- 
ment — perforation of the ventricular septum, patency of the foramen 
ovale or the ductus arteriosus, and stenoses of other orifices. 

Owing to the increased force the right auricle must exert in pro- 
pelling its contents through the stenotic tricuspid orifice, the walls 
of this chamber hypertrophy and later dilate, for the myocar- 
dium weakens under the incessant stress, so that the auricle be- 
comes habitually overfilled by residual blood, and, in most instances, 
overdistended by a systolic reflux stream from the right ventricle, due 
to concurrent tricuspid incompetence. Most extraordinary enlarge- 
ment of the auricle and thinning of its walls are sometimes observed 
as the result of these several factors. The venous obstruction 
depending upon auricular failure has already been described. (See 
p. 444.) The effect of pure tricuspid stenosis is to diminish the size 
of the right ventricle, but, as a matter of fact, this chamber is nearly 
always found to be hypertrophied and dilated, in consequence of an 
attendant mitral lesion, which also accounts for the pulmonary con- 
gestion, when this exists. Arterial anemia develops should the 
right ventricular output of blood be inadequate for the needs of the 
pulmonary circulation, the left side of the heart, and the greater 
blood circuit. 

Physical Signs. 1 — Inspection. — Chronic cyanosis, well-defined 
turgescence of the surface veins, and persistent dropsy are most 
constant, yet not pathognomonic, signs of tricuspid obstruction. 
Assuming that the tricuspid orifice does not leak, there is jugular 
distention, unattended by systolic (positive) pulsation, though a 
presystolic (negative) flicker is sometimes visible should the force 
of the right auricle be sufficient to propel a backward venous wave. 

Palpation. — Occasionally a short, purring, presystolic thrill, end- 
ing in a sharp, systolic impulse, is appreciable over the xiphoid ap- 
pendix, but there is no epigastric throbbing so long as the right 
ventricle does not hypertrophy. The edge of the liver is palpable 
and, rarely, pulsatile below the right costal arch, and the skilful 
use of the kymograph may show a presystolic hepatic pulse wave, 
if the right auricle be hypertrophied (Mackenzie) . The pulse in 

1 For the purpose of description, it is thought best to give the signs of a pure 
tricuspid stenosis. The reader should appreciate, however, that in actmal 
practice this rare lesion, if met with at all, is nearly always attended by other 
valvular defects — by mitral stenosis in fully 90 per cent, of cases. Isolated 
tricuspid stenosis made up but about 7 per cent, of Herrick's 154 collected 
records of this affection. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 479 

the radials may exhibit no deviation from normal, or the beats 
may be accelerated, arhythmic, small, and forceless. 

Percussion. — Right auricular enlargement accounts for consider- 
able extension of cardiac dulness at the base, particularly upward 
and to the right of the sternum. Hepatic dulness is increased 
commensurately with the existing degree- of hepatic engorgement. 

Auscultation. — A short, rough presystolic murmur, ending in a 
sharp first sound and restricted to the tricuspid area, is heard in 
obstruction of the tricuspid orifice. The punctum maximum of this 
murmur, which is not propagated thence, corresponds variously 
to the base of the ensiform or to either edge of the sternum, and, as 
in its mitral equivalent, the sound may be either strictly presystolic 
in time, or it may begin directly after the second sound, running 
through the entire diastolic period with a distinct crescendo just 
before the first sound. The cardiac tones at the base are enfeebled, 
should there be anemia of the pulmonary circuit, and, consequently, 
reduction' in the volume of blood within the left heart. 

Diagnosis. — A presystolic murmur and a sharp first sound in the 
tricuspid area, with enlargement of the right side of the heart, mean 
stenosis of the tricuspid orifice, provided that it is possible to exclude 
concomitant mitral obstruction (q. v.). The frequent coexistence 
of the latter lesion, which masks the tricuspid signs, largely accounts 
for the common failure to recognise tricuspid stenosis during life. 
Corroborative evidence of tricuspid stenosis consists of cyanosis, 
edema, hepatic enlargement, turgid pulsating jugulars, and a presys- 
tolic thrill over the ensiform. According to the elder Broadbent, 
in the face of signs indicating pure mitral stenosis, the presence of 
extensive and persistent dropsy is sufficient grounds for believing that 
the tricuspid orifice is likewise obstructed. 

PULMONARY STENOSIS 

Clinical Pathology. — This very rare defect is almost invariably 
of congenital origin, being the most frequent form of valvular disease 
attributable to developmental imperfection or to fetal endocarditis. 
Ordinarily, the narrowing is due to adhesion of the cusps and con- 
traction of the muscular sphincter, with more or less induration, 
thickening, and rigidity of the leaflets; but vegetative excrescences, 
in the exceptional case, may be virtually the sole cause of the obstruc- 
tion. Or the stenosis may implicate the conus arteriosus, whose 
walls are thickened and indurated by a fibroid myocarditis excited 
by the extension of a primary endocardial inflammation. Rarely, 
endarteritic obstruction of the pulmonary artery is the initial seat of 



480 PHYSICAL DIAGNOSIS 

the stenosis, and in some instances a fault of development results 
in the virtual occlusion of the first part of this vessel and also 
of the pulmonic orifice. In congenital cases the valvular defect is 
generally associated with other antenatal malformations, such as 
patency of the ductus arteriosus or the foramen ovale, and perforation 
of the interventricular septum; frequently the tricuspid orifice is 
likewise obstructed; and, from their very nature, many of the lesions 
causing pulmonary stenosis also cause incompetence of this valve. 
In the few recorded examples of acquired pulmonary stenosis benign 
and malignant endocarditis, gumma, and injury to the precordia 
have figured as the exciting causes. In endocarditic stenoses the 
acute specific infections, and especially the eruptive fevers, appear 
to be more active factors than rheumatism; this is equally true of 
regurgitant lesions at the pulmonic orifice, and in its relative insus- 
ceptibility to rheumatic valvulitis the pulmonic valve differs from the 
valves of the other cardiac orifices. In a pure pulmonary stenosis 
of moderate degree hypertrophy of the right ventricle is the primary, 
if not the only, structural change induced, but if the obstruction be 
extreme, or if it be combined with regurgitation, ventricular dilatation 
and relative tricuspid leakage soon supervene. This, of course, 
leads to embarrassment of the venous flow to the right auricle, the 
evidences of which have been sufficiently considered in a preceding 
paragraph. Pulmonary stenosis, whether congenital or acquired, 
is regarded as a predisposing cause of tuberculosis of the lungs, 
whose blood-supply and nutrition are interfered with by the obstruc- 
tion to the blood flow from the right ventricle. 

Dilatation of the pulmonary artery, the orifice remaining of normal 
size, establishes a condition of relative pulmonary stenosis. 

Physical Signs. — Inspection. — Striking cyanosis, urgent dyspnea, 
and extensive venous turgescence commonly attend pulmonary 
stenosis of the congenital type, but in acquired cases with adequate 
compensation the breathing is not greatly embarrassed, anemic 
pallor is more conspicuous than cyanosis, and the other consequences 
of venous obstruction are not likely to become prominent. The 
epigastrium heaves systolically with undue force, owing to the impact 
of the hypertrophied right ventricle, and most writers speak of pre- 
cordial bulging from the same cause. 

Palpation. — The hand applied to the base of the heart appreciates 
a systolic thrill of variable quality and of maximum intensity in the 
pulmonic area, while palpation over the subcostal angle shows that 
the right ventricle is contracting with excessive force. 

The pulse in the radials, though prone to become accelerated, 



DISEASES OF THE CARDIOVASCULAR SYSTEM 48 1 

small, and arhythmic, gives no specific indication of the valvular 
lesion under consideration. 

Percussion. — An extension of cardiac dulness, relating primarily 
to right ventricular hypertrophy and later to right auricular dilatation, 
is an important corroborative sign of pulmonary stenosis. The 
hepatic area does not increase in size until the supervention of venous 
engorgement of the liver. 

Auscultation. — Pulmonary stenosis creates a systolic murmur 
having its point of maximum intensity in the second and third inter- 
spaces at the left sternal border, and propagated thence upward 
toward the left clavicle, but not into the arterial trunks of the neck 
(Fig. 159). If the bruit be intense, its area of audibility may extend 
over a considerable part of the anterior chest- wall, but invariably it is 
more distinct on the left than on the right side, being conducted along 
the pulmonary artery and its branches rather than by the aorta. The 
murmur of pulmonary obstruction ordinarily is intense, rough, and 
superficial, effectually masking the pulmonic first sound, though 
exceptionally it is a feeble, soft, and distant tone. The pulmonic 
second sound is either muffled and impure, or entirely suppressed, 
but the sounds in the aortic area are likely to remain clear and 
distinct. 

Diagnosis. — The direct diagnosis of pulmonary stenosis rests 
upon these cardinal signs: a harsh systolic murmur, perhaps attended 
by a thrill, in the pulmonic area, and thence reflected upward toward 
the clavicle, but not conducted into the neck; enfeeblement of the 
pulmonic second sound; and evidences of right ventricular hyper- 
trophy. Information corroborative of this lesion includes, in con- 
genital cases particularly, the presence of cyanosis, dyspnea, and 
venous turgescence, and, in numerous' other instances, diminished 
volume and increased rate of the pulse, together with the demonstra- 
tion of a tuberculous infection of the lungs and of systemic evi- 
dences thereof. 

Only exceptionally does a systolic murmur in the pulmonic area 
mean organic stenosis of the pulmonic orifice, for this " region of 
auscultatory romance," as Balfour so aptly describes it, is the site 
of numerous bruits, both functional and organic, which have nothing 
whatever to do with a structural defect of the right semilunar valve- 
cusps. 

Anemia is by far the most common factor of a pulmonary systolic 

murmur, and a bruit of this nature is likely to be soft and low-pitched, 

attended by a venous hum in the neck and by a sharp pulmonic 

second sound, but unattended by cvanosis and by hypertrophy of 

31 



482 PHYSICAL DIAGNOSIS 

the right ventricle; furthermore, an anemic murmur is peculiarly 
affected by postural changes, and, naturally, disappears when the 
patient's blood impoverishment improves. 

In relative ptdmo7tary stenosis, due to dilatation of the pulmonary 
artery, the pulmonic systolic murmur is more often soft and quiet 
than loud and harsh, the right heart is not enlarged, cyanosis is 
wanting, and the patient's appearance indicates malnutrition, 
debility, and general muscular flabbiness. 

A cardiorespiratory murmur is frequently referred to the pulmonic 
area, but a sound of this sort resembles a sudden brief puff or whiff 
of air, lacks the harmonious vibratory tone of a genuine bruit, and is 
exaggerated by respiratory phases and by changes in posture favorable 
to intimate contact between the heart and the lung. As a rule, a 
cardiorespiratory murmur is systolic, though it may be diastolic; 
and while not incompatible with health, it often accompanies 
emphysema, in which affection both cyanosis and right ventricular 
hypertrophy may exist. 

The conus arteriosus may be the seat of a systolic bruit, audible 
over the pulmonic area, should this part of the right ventricle be 
uncovered by a recession of the anterior edge of the left lung, due, 
for example, to its deficient inflation. In consequence of this each 
systole of the heart thrusts the conus directly against the thoracic 
wall, thereby flattening its anterior surface and agitating within the 
chamber blood eddies conducted forward by the blood-current. 1 
This variety of murmur usually disappears when the patient takes a 
deep breath and holds it, thus intervening a cushion of inflated lung 
between the heart and the chest-wall. In addition to this point, it 
should be remembered that a functional murmur generated within 
the ventricular cone produces no enlargement of this chamber, nor 
is it attended by dyspnea or cyanosis. 

Atheroma of the aortic arch and true aortic stenosis must be reckoned 
with as common factors of a systolic murmur in the pulmonic area, 
but the murmurs attending both these lesions are distinctly conducted 
into the carotid arteries — a fact alone sufficient to exclude pulmonary 
stenosis, though the differentiation is made doubly sure by detecting, 
in aortic atheroma, left ventricular hypertrophy, a ringing aortic 
second sound, and arterial sclerosis; and in aortic stenosis, left 
ventricular hypertrophy, a muffled or absent aortic second sound, 
and a pulsus tardus. 

The murmur of mitral regurgitation may be clear and distinct in 

1 Very gentle pressure upon the conus is sufficient to excite a murmur therein, 
as shown by the experiments of Thayer and MacCallum. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 483 

the pulmonic area, but the mitral murmur, though timed like that of 
pulmonary stenosis, is conducted toward the left axilla and supple- 
mented by an accentuated pulmonic second sound, and in cases of 
organic leakage, the left ventricle becomes obviously enlarged, as 
well as the right side of the heart. 

Aneurism of the aortic arch is sometimes mistaken for pulmonary 
stenosis, inasmuch as a rough systolic murmur and thrill are common 
to both lesions. If aneurism be suspected, one should search for 
the more distinctive signs of this condition, such as systolic pulsation 
and diastolic shock over a circumscribed dull area, a systolic 
carotid bruit, the aneurismal second sound, tracheal tugging, pulse 
inequality, and evidences of mediastinal pressure. 

That rare lesion, stenosis of the pulmonary artery, generates a 
murmur indistinguishable from that of pulmonary obstruction, 
and, if the vessel be sufficiently stenosed, right ventricular hyper- 
trophy and its sequels also supervene. In venturing to differentiate 
these two conditions, the character of the pulmonic second sound is 
a valuable guide, since this tone, enfeebled in stenosis of the orifice, 
is accentuated in stenosis of the artery, owing to the high pressure 
therein. The presence of systolic pulsation at the sternal end of 
the second left intercostal space and impaired resonance in this 
area are other findings in favor of arterial obstruction, and a similar 
significance attaches to the demonstration, in the upper part of the 
left lung, of a cirrhotic or tuberculous process to which constriction 
of the artery can be attributed. 

The signs of a perforate interventricular septum are compared with 
those of a pure pulmonary stenosis on page 487. 

PULMONARY REGURGITATION 

Clinical Pathology. — Leakage at the pulmonic orifice arises 
in consequence of structural deformities of the valve or of undue 
stretching of the muscular sphincter, either of which defects is 
responsible for faulty approximation of the valve borders, and hence 
for the escape of blood from the pulmonary artery into the right 
ventricle during its diastole. Pure pulmonary regurgitation as an 
isolated lesion is the rarest variety of valvular disease, and, in its 
acquired form, is most commonly met with in young adults. Organic 
pulmonary regurgitation depends upon structural deformities of the 
valve mechanism analogous to those existing in aortic regurgitation, 
these changes being due to acute endocarditis more often arising in 
connection with the eruptive fevers and septic states than as the 
result of rheumatism; exceptionally the valve is damaged by pro- 



484 PHYSICAL DIAGNOSIS 

gressive sclerosis. In congenital cases fusion of two of the valve- 
leaflets is the common factor of the incompetence, and with this lesion 
other developmental imperfections of the cardiac orifices and cham- 
bers are ordinarily associated. Relative pulmonary regurgitation, 
due to dilatation of the pulmonic orifice by abnormally high pressure 
within the pulmonary artery, is not of common occurrence, for the 
pulmonic ring, being firm and resistent, only exceptionally stretches 
under the stress of arterial hypertension. When the orifice enlarges 
so as to allow diastolic leakage of blood from the pulmonary artery 
into the right ventricle, either mitral disease or some indurative 
affection of the lungs should be looked for as the underlying cause 
of the intrapulmonary hypertension. The pulmonary artery, as 
well as the orifice, is more or less dilated and prone to undergo 
atheromatous changes. Exceptionally, relative pulmonary regurgi- 
tation indicates a purely functional rise of blood-pressure in the 
pulmonary artery. 

Physical Signs. — Inspection. — There are no distinctive visual 
signs of this rare lesion, which, in its pure, organic form is attended 
by cough, dyspnea, cyanotic pallor, and other evidences of disordered 
pulmonary blood-supply and of arterial anemia; in the vast majority 
of instances the subject's appearance betrays engorgement of the 
lungs and general venous stasis incident to concomitant left-sided 
valvular defects and to secondary tricuspid incompetence. Systolic 
pulsation in the epigastrium and, perhaps, in the interspaces at the 
right sternal edge is visible when there is considerable enlargement 
of the right ventricle. 

Palpation. — Occasionally it is possible to feel a basic diastolic 
thrill, having its greatest distinctness in the pulmonic area. Tumul- 
tuous throbbing in the epigastric region, and, not infrequently, a 
systolic, non-expansile hepatic pulsation, accompany the stage of 
right ventricular hypertrophy. 

The pulse is not at all characteristic, though, as a rule, the radials 
are of small volume, low tension, and erratic rhythm. 

Percussion. — Cardiac dulness is increased, especially to the right 
of the sternum, to an extent proportionate to the enlargement of the 
right ventricle, and, sooner or later, right-sided basal impairment 
due to dilatation of the right auricle supervenes. Until the tension 
within this chamber becomes excessive, there is no enlargement of 
the hepatic area. 

Auscultation. — Pure pulmonary leakage gives rise to a soft (rarely, 
harsh and rasping) diastolic murmur in the pulmonic area, from 
which point of greatest intensity the bruit can be traced downward 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



485 



along the left sternal border and toward the apex of the heart. The 
pulmonic second sound is enfeebled or lost, but the character of the 
other cardiac tones undergoes no primary alteration. 

Diagnosis. — A diagnosis of pulmonary regurgitation is justified 
by the following combination of physical signs: a diastolic pulmonic 
murmur conducted down the sternum, impairment or obliteration 
of the pulmonic second sound without notable alteration in its aortic 
equivalent, right-sided cardiac enlargement, and a frequent, small 
arterial pulse. Ultimately, to these findings are to be added those 
relating to secondary tricuspid leakage and general venous engorge- 
ment. 

Relative pulmonary regurgitation, of the type excited by the excessive 
engorgement of the lungs secondary to mitral stenosis, accounts for 
a diastolic pulmonic bruit described by Steell as "the murmur of 
high pressure in the pulmonary artery." This murmur is distin- 
guished, aside from its association with a primary mitral defect, by 
a most evanescent character, for the sound appears and vanishes 
according to pressure variations within the pulmonary artery. The 
pulmonic orifice may be temporarily incompetent in consequence of 
pulmonary hypertension induced by violent exercise and by deep 
breathing. Cabot refers to persons in perfect health who were able, 
by prolonged holding of the breath, to produce a short, high-pitched 
diastolic murmur, best heard in the second or third left interspaces, 
and disappearing when respiration was resumed. The transient 
occurrence and the method of producing a functional murmur of this 
sort are sufficient denial of its organic nature, apart from the lack of 
consecutive structural changes in the heart. 

Aortic regurgitation can beget a soft diastolic bruit having great 
intensity in the pulmonic area, and thence propagated downward 
like the murmur of pulmonary regurgitation. Corrigan's disease, 
however, is accompanied by an ox-heart, throbbing arteries, the 
water-hammer pulse, an obscure aortic, and a sharp pulmonic, 
second sound; while pulmonary regurgitation is associated with 
right ventricular enlargement, quiet arteries, a small pulse, a feeble 
pulmonic, and unimpaired aortic, second sound. 

CONGENITAL CARDIAC DISEASE 

Clinical Pathology. — Of the numerous forms of congenital heart 
disease, pulmonary stenosis, defects of the interventricular septum, 
and patency of the ductus arteriosus are of clinical interest, owing to 
their relative frequency as antenatal lesions and because they offer, 



486 



PHYSICAL DIAGNOSIS 



when existing singly, reasonably good opportunities for a diagnosis 
during life. Of purely pathologic interest are the structural changes 
relating to a patent foramen ovale (Fig. 181), and to absence of the 
septa between the auricles, the ventricles, or both. Congenital 
lesions of the tricuspid, mitral, and aortic valves have been suffi- 
ciently discussed under Valvular Disease. 

Congenital malposition of the heart may take the form of dextro- 
cardia, in which condition the heart lies on the right side of the 
thorax, thus giving a " mirror picture" of the normal physical signs, 



Right auricular wall 




Right ventricle 



Fig. 181. — Patent foramen ovale (Philadelphia General Hospital). 



and in this anomaly there is generally a corresponding transposition 
of the abdominal viscera, the combined abdominothoracic dislocation 
constituting a situs viscerum inversus. Persistence of the heart in 
its normal fetal position in the median line of the thorax is known 
as mesocardia. Ectopia cordis, or the situation of the heart outside 
the thorax, occurs in three forms: pectoralis, in which the heart, 
covered by the pericardium and integument or by the pericardium 
only, bulges through a midsternal fissure; cervicalis, or a displacement 
of the heart upward into the neck close to the lower jaw; and 
abdominalis, or subphrenic displacement of the heart downward into 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



487 



the abdominal cavity. The last of these anomalies is not necessarily 
incompatible with many years of life, but in the other two postnatal 
existence, if at all possible, is of brief duration. 

Anomalies of size comprise congenital hypertrophy and atrophy, 
the former ordinarily being the result of fetal endocarditis, and the 
latter part and parcel of a general cardiovascular hypoplasia some- 
times incident to chlorosis and to lymphatism. 

Transposition of the aorta and pulmonary artery, the former having 
a right, and the latter a left, ventricular origin, is a peculiarity of 
development commonly associated with a persistent arterial duct 
between the two transposed arterial channels. Communication of 
both aorta and pulmonary artery with the same ventricle, with or 
without malformation of the septa and the duct of Botallo, is a type 
of anomaly somewhat more common than the foregoing. 

Physical Signs.— Congenital pulmonary stenosis, like the acquired 
form, generates a systolic murmur most intense in the pulmonic 
area, and thence transmitted toward the left clavicle, but not into the 
neck, of which leading sign a systolic basic thrill and hypertrophy of 
the right ventricle are strongly confirmatory. (See p. 479.) 

A pervious interventricular septum is commonly combined with 
the foregoing lesion, and in this event its auscultatory signs are usually 
so overshadowed by the pulmonary murmur as to render it unrecogni- 
zable. An isolated ■ septal perforation may be identified by finding 
a loud and harsh systolic bruit with its punctum maximum in the 
fourth left interspace, between the sternum and the midclavicular line, 
and highly characteristic in that it is a continuous sound running 
through the entire cardiac cycle (Rogers' murmur). A systolic 
thrill is not uncommonly palpable. During systole the intensity 
of this murmur is increased and the pitch raised, while with diastole 
it dwindles to a low, though distinct, rumble. The bruit has been 
likened to the rasping sound of a grinder's wheel when a knife is 
being sharpened. Hypertrophy of the right ventricle is the 
ordinary consequence of this defect, which, save for the absence of 
pulmonary congestion, accounts for objective phenomena like those 
of mitral stenosis. 

Persistence of the ductus arteriosus has been recognized during life 
by the detection of a late systolic murmur, audible in the pulmonic 
area, and propagated toward the apex. This murmur, which appears 
immediately to follow, rather than exactly to coincide with, the first 
sound, is generally distinguished by a high pitch, by considerable 
intensity (especially during inspiration), and by prolonged duration. 
Accentuation of the pulmonic second sound and the presence of 
right ventricular hypertrophy are important secondary signs, while 



PHYSICAL DIAGNOSIS 

paradoxic weakening of the pulse during inspiration, and systolic pul- 
sation in the second left interspace also have been observed. 

Patent foramen ovale, if an isolated lesion, may be wholly symp- 
tomless; under no circumstance does a pervious interauricular 
septum give rise to a distinctive clinical picture. 

Diagnosis. — Congenital disease of the heart is indicated by a 
history of cyanosis from birth, — a "blue baby," in lay vernacular, — 
with dyspnea and physical blemishes, such as dwarfed stature 
and clubbed fingers and toes. As a rule, physical exertion de- 
cidedly deepens the blueness. Given these general indications, the 
discovery of one of the above groups of signs may lead to the 
diagnosis of the precise defect. The very name, morbus cceruleus, 
applied to congenital heart lesions as a class, denotes the im- 
portance of cyanosis as a sign of these affections. It probably 
means imperfect aeration of the blood, despite attempts made to 
attribute it chiefly to venous stasis and to commingling of the 
arterial and venous currents. Cyanosis is most common and 
usually most striking in pulmonary stenosis, but it is by no means 
restricted to this lesion, and this is likewise true of the other signs 
just noted. 

ANEURISM OF THE AORTA 
ANEURISM OF THE THORACIC AORTA 

Clinical Pathology. — Atheroma of the aorta and high blood-pres- 
sure are the almost invariable essential factors of aneurism of the 
thoracic aorta, which is prone to occur in men during the third and 
fourth decades of life, when, as Coats expresses it, "the period of 
greatest bodily vigor overlaps the period of beginning atheroma." 
In other words, the lesion develops most commonly at that time of 
life when the cardiac force is greatest, while the vessel is impaired 
by a degenerative process, which, being incipient and, therefore, 
unattended by compensatory endarteritis, damages without attempt- 
ing to repair its inroads. Syphilis is by far the commonest cause of 
the arterial degeneration, though bacterial toxins, infected emboli, 
plumbism, gout, and alcohol are also accredited factors of sclerosis 
whereby the artery is likely to yield, either gradually under the tax 
of persistently high blood-pressure, or suddenly in consequence of 
a violent muscular strain, as from lifting a heavy weight or from a 
hard fit of coughing. Under these conditions one or more of tht 
impaired arterial coats may give way at the site of a focal or circum- 
scribed atheroma, with subsequent pouch-like bulging of the arterial 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



489 



wall and the formation of a saccular aneurism. In diffuse, fusiform 
aortic aneurism wide-spread atheromatous enfeeblement of the 
vessel-wall, without especially vulnerable local patches of degenera- 
tion, is to be assumed. 

Of all cases of aortic aneurism, approximately three-fourths affect 
the thoracic division, the favorite site being the ascending portion of the 
arch, after which, in order of incidence, the transverse and descending 
portions, and the descending thoracic aorta are implicated (Fig. 182). 
Saccular aneurism produces the clearest physical signs, and is by 
far the most common type met with clinically, this variety constituting 
about 95 per cent, of the 570 cases of thoracic aneurism collected by 




III. Transverse arch 

IV. Descending arch 



V. Descending thoracic 
aorta 



II. Abdominal aorta 



Fig. 1 



Relative site incidence of aortic aneurism. 



Hare and Holder. Fusiform aneurismal dilatation of the aorta 
(Fig. 184) may attain a huge size without attracting attention. As 
a rule, there is but a single sac, which may be as small as a marble 
or as large as a football; exceptionally, the aorta is found to be 
studded with multiple sacculations. The changes in the wall of the 
aneurism comprise thinning and ultimate disappearance of the media 
from atrophy and destruction of the muscular and elastic fibers, 
and, subsequently, fibrous thickening of the intima and adventitia, 
the latter coat virtually forming the wall of the sac and frequently 
being matted by adhesions to neighboring structures. Eventually 



49° 



PHYSICAL DIAGNOSIS 



every vestige of the three arterial coats may disappear and a sac 
be constructed of the surrounding tissues— -false aneurism, in con- 
trast to a true aneurism, in which at least one arterial coat persists. 
Or, a dissecting aneurism may arise, should a breach be torn in the 
intima through which the blood penetrates to bore a channel 
between the outer coats of the vessel; and if such a channel, 



Right clavicle > 

First rib 

Innominate artery 

Left common carotid 
artery 

Aneurismal sac 

Left subclavian artery 



Ascending aortic arch 
Pulmonary artery 



Conus arteriosus _ 




Descending aortic arch 



Right ventricle 



Fig. 183. — Saccular aneurism of the aortic arch (Philadelphia General Hospital). 



instead of draining into the surrounding parts, leads back into the 
aorta by another opening in the intima, the curious anomaly termed 
double aorta is formed. An arteriovenous aneurism, effecting chiefly 
the peripheral vessels (Fig. 185), consists of an abnormal com- 
munication between an artery and a vein, the connection between 
the two vessels being either direct {aneurismal varix) or established 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



491 



by an intervening sac {varicose aneurism). A laminated fibrinous 
clot usually occupies the interior of the aneurismal sac, which, 
indeed, may be wholly obliterated thereby, though rupture of the 
sac is the ordinary termination. This occurs most frequently into 
the left pleural cavity, and then, in this order of incidence, into 
the pericardium, right pleura, esophagus, and larger air-passages; 
less commonly the superior vena cava, the pulmonary artery, or 
the heart is penetrated, or the rupture may be external. 



Trachea 



Focus of soften 
ing 



Ascending aortic 
arch 
Pulmonary 
artery 
Right auricle 



Right ventricle 




Left common 
carotid artery 

Left subclavian 
artery 



Aneurismal sac 



Focus of 
softening 



;ft auricle 



Left ventricle 



Fig. 184. — Fusiform aneurism of the aortic arch (Jefferson Hospital Laboratories). 



Some aneurisms remain symptomatically latent for a long period, 
but ordinarily the enlarging sac encroaches upon the surrounding 
structures, displacing them and exciting therein various mechanical, 
inflammatory, and necrotic changes, due to compression. The 
bronchi and lungs are particularly liable to damage thus inflicted- 
which takes the form of bronchial ulceration, necrosis, stenosis, and 
ectasis, and of pneumonic, fibroid, and gangrenous processes in the 



492 



PHYSICAL DIAGNOSIS 



lungs; erosion of the bony thorax — ribs, sternum, vertebrae — is not 
uncommon; and pressure phenomena relating to the gullet and to 
the nerves and great vessels of the mediastinum are familiar findings. 
Aortic aneurism is commonly attended by cardiac hypertrophy, but 
it is questionable if the aneurism, per se, is the primary factor of the 
enlarged heart. 

The study of thoracic aneurism is facilitated by localizing the 
lesion to some one of the following four clinical divisions of the 

artery: {a) ascending arch, or that por- 
tion of the vessel extending from the 
base cf the left ventricle to the orifice 
of the innominate artery, and corre- 
sponding to the two anatomic portions 
termed the ascending aorta and the 
first part of the aortic arch; (b) trans- 
verse arch, between the innominate and 
the left subclavian arteries and includ- 
ing their mouths; (c) descending arch, 
lying between the left subclavian and 
the fourth thoracic vertebra; (d) de- 
scending thoracic aorta, occupying the 
posterior mediastinum between the 
fourth thoracic vertebra and the aortic 
opening in the diaphragm at the level 
of the twelfth thoracic vertebra. The 
surface topography of the thoracic 
aorta has been given on page 319. 

Aneurisms of the ascending aortic arch 
usually arise from the convexity of the 
vessel above the pericardial limit, and 
pass forward and to the right, appear- 
ing in the neighborhood of the second 
and third right intercostal spaces and 
the sternum (Fig. 187), or they affect 
the concavity of the aorta, and give rise 
to physical signs along the left sternal 
border. Or the dilatation may be intra- 
pericardial, arising at or immediately above the sinuses of Valsalva, 
in which case rupture into the pericardium, causing instant death, is 
probable before the aneurism reaches a large size. Aneurisms of 
the ascending arch tend to cause striking cardiac displacement, 
to stretch the aortic ring so as to set up relative aortic leakage, and 




Fig. 185. — Arteriovenous aneur- 
ism (Jefferson Hospital). 



DISEASES OF THE CARDIOVASCULAR SYSTEM 493 

tc compress the superior (rarely, the inferior) vena cava, the sub- 
clavian vessels, the pulmonary artery, and the right recurrent laryn- 
geal nerve. Rupture may take place into the right pleura, the 
pericardium, or, exceptionally, into the superior vena cava. 

Aneurisms of the transverse arch commonly spring from the pos- 
terior wall of the aorta, and are more likely to extend backward 
toward the spine or to invade the pleurae, than to press forward and 
erode the chest-wall beneath or alongside the sternum. Implication 
of both the ascending and transverse portions, which sometimes 
occurs, results in a tumor of extraordinary dimensions whose exten- 
sion takes an upward and outward direction (Fig. 188). The struc- 
tures particularly exposed to compression by an aneurism of the 
transverse arch are the trachea, esophagus, left bronchus, and left 
recurrent laryngeal nerve, and, less frequently, the sympathetic nerve 
and the thoracic duct. When the sac compresses, communicates 
with, or lies between the innominate, left common carotid, or left 
subclavian arteries, corresponding alterations take place in the carotid 
and radial pulses (q. v.). The potential causes of death in this type 
of aneurism include pressure-asphyxia, secondary pulmonary com- 
plications, and hemorrhage from rupture of the sac into the trachea, 
left bronchus, pleurae, or posterior mediastinal space. 

Aneurisms of the descending arch extend to the left and backward, 
and if they reach the surface, appear alongside the spine in the left 
interscapular region. The accompanying illustration (Fig. 189) 
shows the conspicuous deformity produced by such a tumor, which, 
owing to its deep situation, must attain an enormous size to cause 
surface signs. Nor are evidences of intrathoracic pressure well 
defined in the average case; the structures most likely thus to sutler 
are the esophagus, the thoracic duct, the spinal nerves, and the 
vertebrae, while less commonly the root of the left lung is compressed. 
Rupture into the esophagus, left pleural sac, or left bronchus, and 
consecutive lesions of the lungs are the ordinary causes of death in 
aneurism of this portion of the aortic arch. 

Aneurisms of the descending thoracic aorta, usually situated just 
above the diaphragm, lie to the left or in front of the lower thoracic 
vertebrae and in close contact therewith. Pressure-erosion of these 
bones, irritation of the spinal nerves, and perhaps compression of 
the esophagus and pleuropulmonary tissues are to be looked for 
when the aneurism does not follow a latent course. Death by rupture 
of the sac into the pleura or the esophagus is the usual outcome of an 
aneurismal dilatation in this situation. 

Physical Signs.— Inspection.— The chest-wall should be carefully 



494 



PHYSICAL DIAGNOSIS 




DISEASES OF THE CARDIOVASCULAR SYSTEM 495 

scrutinized with the object of finding an area of abnormal systolic 
pulsation, which is always highly suggestive of aneurism. The favorite 
sites of such pulsations are the anterior surface of the thorax, between 
the clavicle and the third rib, near the sternal border, especially on the 
right side (ascending arch) , the suprasternal notch and the right supra- 
clavicular space (transverse arch; innominate artery), and the left 
interscapular region near the spine (descending arch) . Feeble pulsa- 
tions — and these are by no means exceptional — are usually discovered 
only by most minute inspection of the questionable area from an 
oblique viewpoint; or by laying the finger-tips over the part and noting 



^i 




Fig. 187. — Aneurism of the ascending aortic arch (Jefferson Hospital). 

their rhythmic elevation with each beat of the heart; or by observing 
that the barrel of a single stethoscope, whose chest-piece is applied 
to an interspace, is periodically tilted by a transmitted throb from 
beneath. On the other hand, sometimes the impulses are so strong as 
to cause an extensive circumscribed heaving of the chest-wall, appar- 
ent at first glance. According to the amount of erosion produced, a 
local bulging or even a definite tumor, each pulsatile, may appear, 
and over the swelling the tissues tend to become brawny, edematous, 
and stained purple or black with suffused blood, while later the sur- 
face structures may break down and a mixture of serum and blood 



496 



PHYSICAL DIAGNOSIS 



trickle from the sac. Figs. 187, 188, and 189 show the deformities 
produced by large aneurismal tumors which have eroded the chest- 
wall. The cardiac apex is crowded below and outside its normal 
site, and may beat tumultously, owing to concomitant hypertrophy. 
Engorged veins upon the chest and upper extremities, edema of one 
arm, cyanosis, dyspnea, unequal pupils, and unilateral sweating are 

other objective phenomena 
whose prominence depends 
upon the degree and situation 
of the mediastinal pressure in 
the individual case. Signorelli 
attaches importance to wast- 
ing of the left sternomastoid 
muscle as a sign (due to nerve 
degeneration from pressure) 
of aneurism of the transverse 
and descending arch. The 
larynx may be immobilized, 
depressed, and displaced to- 
ward the left by a large an- 
eurism of the ascending part 
of the aortic arch. (Boinet.) 
X-ray examination with the 
fluoroscope is a great diag- 
nostic aid, for it may clearly 
reveal a shadow to the right, 
to the left, or on both sides of 
the sternum in aneurism of 
the aortic arch, and in aneur- 
ism of the descending tho- 
racic aorta this method of ex- 
amination often is the only 
means of securing definite data. Moreover, the x-rays show the 
extent of the cardiac dislocation consequent to pressure by the 
tumor, and, if the sac be resilient and comparatively clot-free, 
expansile pulsations are unmistakably shadowed upon the fluo- 
rescent screen. 

Palpation. — The extent and. character of the pulsation are best 
judged by palpation, which also may discover an abnormal throb too 
feeble to attract the eye. The palm of the hand appreciates either 
an obscure indefinite pulsation or a powerful lifting or heaving impact 
over the aneurism, according to its size and distance from the chest- 




Fig. 188. — Aneurism of the ascending 
and transverse aortic arch and innominate 
artery (Jefferson Hospital). 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



497 



wall. If the latter be eroded, so that the sac projects externally 
as a tumor, a trio of valuable signs becomes available — expansile 
pulsation, diastolic shock, and systolic thrill. The expansile pulsa- 
tion is due to the uniform distention of the sac with blood, and the 
sharp, short diastolic shock immediately following is produced by the 
sudden recoil of the aortic wall after its systolic distention. The 
thrill often associated with these two signs corresponds to systole and 
has a peculiar vibratory quality. The foregoing findings, practi- 
cally pathognomonic of aneurism, indicate a resilient sac having com- 
paratively fluid contents, and a tumor of this sort is not unlikely to 
be so soft and fluctuating that any manipulation, save the gentlest, 



Aneurismal tumor 
Displaced left scapula 




Fig. 189. — Aneurism of the descending aortic arch (Jefferson Hospital). 



is interdicted, for fear of rupturing the fragile wall. These signs, 
of course, are not found over an aneurismal tumor having a rigid, 
thick wall, reinforced by a laminated clot so large and firm as to 
interfere with the generation and conduction of vibrations and to 
impair the sac's mural elasticity. When these conditions rule, the 



32 



49 8 



PHYSICAL DIAGNOSIS 



consistence of the tumor will be firm and hard, and its pulsation a 
lifting impact. Tracheal tugging, though presumptive evidence of 
aneurism, especially of the transverse arch, is not distinctive, for 
a similar systolic depression of the windpipe is sometimes seen in 
simple dilatation of the aorta and in mediastinal neoplasm. (See 
p. 336.) An inversion of Oliver's sign, or a rhythmic elevation of 
the trachea with systole, has been described by Hirtz in aneurism 
springing from the convexity of the aortic arch. Aside from the 
spontaneous pain the patient suffers, local tenderness and sometimes 
excruciating radiations of pain are commonly provoked by pressure 
over the site of the aneurism: when, for example, the descending 
arch is implicated, tapping the upper thoracic vertebrae sets up 
aching of the spine and acute lancinating pain radiating thence over 
the left side of the thorax. 

The pulse in the radial and carotid arteries is significantly modified 
by aneurisms of the ascending and transverse portions of the aortic 
arch, the nature of these alterations corresponding essentially to the 
situation of the sac. Aneurism of the ascending arch, situated between 
the aortic orifice and the innominate artery, but not compressing the 




Fig. 190. — Synchronous sphygmographic tracings of the right and the left carotid 
arteries in a case of innominate aneurism. (Tracing by Dr. G. Bachmann.) 



latter, obviously modifies both radials identically, and under this cir- 
cumstance the right and left pulses at the wrist are perfectly synchro- 
nous and equal, though they are both likely to be delayed in comparison 
with the precordial impulse, and unnaturally full between beats, 
while the pulse- waves are of moderate amplitude, prolonged duration, 
and deliberate subsidence. Inequality in the time, volume, and ten- 
sion of the two radial pulses suggests pressure upon, or obstruction 
within, either the innominate artery or the left subclavian artery by 



DISEASES OF THE CARDIOVASCULAR SYSTEM 499 

an aneurism attached to some part of the transverse arch. If the 
innominate be obstructed or compressed by an aneurism lying 
between the orifice of this trunk and the left subclavian, the right 
radial pulse will be later, smaller, weaker, and softer than the left. 
If the left subclavian artery leads directly from an aneurismal sac, 
or if it be compressed by a dilatation of the transverse arch well to 
the left of the innominate's origin, the left radial pulse will exhibit the 
alterations just noted. The sphygmogram reproduced above graphic- 
ally illustrates these pulse differences, so suggestive of aneurismal 
pressure (Fig. 191). Pulse changes in the carotid arteries like 
those affecting the radials also occur, inasmuch as innominate 
obstruction must check and diminish the current within the right 
common carotid and its branches, while factors acting on the left 
subclavian artery must similarly affect the adjacent left com- 
mon carotid. It is quite apparent that an aortic aneurism distal 
to and well removed from the left subclavian artery cannot influence 
the pulses in the arms and wrists, though both femoral beats may be 




Fig. 191.— Simultaneous sphygmographic tracings of the carotid artery and of an 
aortic aneurismal sac. (Tracing by Dr. G. Bachmann.) 

enfeebled and delayed, yet synchronous. Osier noted complete 
abolition of pulsation in the abdominal aorta in aneurism of the 
descending arch. In addition to noting the above important pulse 
deviations, one should not fail to study the condition of the arterial 



500 PHYSICAL DIAGNOSIS 

walls, inasmuch as arteriosclerosis of the peripheral vessels is in 
favor of aneurism. 

Percussion. — As an aneurism approaches the chest-wall percussion 
resonance is thereby impaired over an area corresponding to the site 
of the sac. Percussion is of unquestionable value in recognizing a 
beginning aneurismal enlargement of the ascending and transverse 
arch, in which an unnaturally broad zone of supracardiac vascular 
dulness, with proportionately increased tactile resistance, is frequently 
appreciable long before other physical signs appear. Later, as the 
sac enlarges, frank dulness, or even flatness, becomes well marked 
over and alongside the manubrium, in aneurisms of the ascending 
and transverse portions; and in the left interscapular region, near 
the spine, when the descending arch is greatly dilated. Obviously, 
a small intrapericardial aneurism lies beyond the range of per- 
cussion, and the same is true of an aneurism of the descending 
thoracic aorta, unless it be of great size. 

Auscultation. — The presence or absence of a murmur over an 
aneurism is of very minor import, for it occurs with great inconstancy 
and is in no wise distinctive. A systolic bruit may be generated 
within an aneurismal sac, or within the aorta lying beyond and 
compressed by the dilatation (Fig. 163, p. 4 01 ) 5 and in some cases 
a precisely similar murmur arises at a stenotic aortic orifice, 
and is transmitted thence into the sac and through the aorta. 
Here may be mentioned DrummonoVs sign: a rhythmic systolic 
whiff sometimes heard at the open mouth of a subject of aortic 
aneurism; Sanson? s sign: a similar sound, audible with a steth- 
oscope applied to the patient's lips; and Glasgow 1 s sign : a systolic 
sound heard over the brachial artery. The foregoing oral signs 
must not be confused with Galvagni's buccal souffle: rhythmic sys- 
tolic interruption of the expiratory sound audible at the subject's 
mouth, in paracardial pleurisy and in dilated hypertrophy of the 
heart, and attributed to the rush of intrapulmonary air columns 
expelled by the impact of the heart. 

The most valuable auscultatory sign of aneurism is an intense and 
low-pitched diastolic sound over the aortic area, and usually audible 
for a considerable distance on both sides of the sternum. This 
distinctive sound is exactly synchronous with the palpable diastolic 
shock, and is probably due not so much to the snap of the aortic 
cusps, as to sudden tension of the aortic wall. A diastolic murmur 
of associated aortic regurgitation is frequently also audible, but 
despite this the aneurismal second sound usually persists, though 
it is modified by the attendant bruit. 



DISEASES OF THE CARDIOVASCULAR SYSTEM 501 

Over the sternum loud tubular breathing is heard should the 
tracheal breath-sounds be conducted to the surface by an aneur- 
ism adjacent to the wind-pipe, while noisy and stridulous breathing 
may mean either stenosis of one of the larger air-passages or 
pressure paralysis of the recurrent laryngeal nerve. In some 
instances examination of the chest gives positive evidence of pul- 
monary atelectasis, consolidation and congestion, and of pleural 
effusion symptomatic of pressure upon a bronchus, the pulmonary 
tissue, the pulmonary veins, and the azygos veins, respectively. 

Diagnosis. — Increase in the transverse vessel dulness and a 
barely palpable systolic pulsation at the level of the second inter- 
space in a hard-working man with rigid arteries, and who con- 
fesses to syphilis or whose blood affords a positive Wassermann 
reaction, are highly suggestive of beginning aneurismal dilatation 
of the first or second divisions of the aortic arch — this, despite no 
murmur, thrill, tumor, nor pressure symptoms. In a case of this 
sort the x-ray sometimes furnishes invaluable positive evidence. 
At a later stage, when the aneurism nears the surface or erodes it, 
an area of circumscribed dulness or a definite tumor, heaving or 
expansile pulsation, a diastolic shock, the aneurismal second sound, 
the tracheal tug, a thrill, and a systolic murmur complete the clinical 
picture. Not only may the pulses of the two sides differ in time and 
in volume, but not infrequently, according to Williamson, there is 
a difference of from 20 to 30 mm. in the blood-pressure of the right 
and left peripheral pulses. The pupil on the side of the lower 
pressure is the larger, MacKinnon has found. 

Pressure symptoms corroborative of these physical signs, and, 
indeed, in some instances the sole evidence of the lesion, are much 
more conspicuous in aneurism of the transverse and descending 
portions of the arch than in aneurism of the ascending part, a fact 
that prompted the elder Broadbent to term the former the 
" aneurism of symptoms" and the latter the "aneurism of physical 
signs." The pertinent symptoms due to pressure vary with the site 
of the compression, but a general summary of such effects may be 
expressed as follows: (a) pain, of boring, anginose, or radiating 
character; (b) dyspnea and dysphagia; (c) cough, bloody expectora- 
tion, huskiness, brassy voice, aphonia, and stridor; (d) inequality 
of the pupils, unilateral sweating, hyperemia, and pallor of the 
face; (e) engorgement of the superficial veins, with edema and suf- 
fusion of the upper extremities, ne.ck, and face; and (/) the second- 
ary lesions of the bronchopulmonary system referred to above. 
Hoesslin has noted stridulous expiration interrupted during dias- 



502 PHYSICAL DIAGNOSIS 

tole as a result of pressure upon the trachea by an aneurismal 
growth. 

Rupture of an aortic aneurism into the superior vena cava, forming 
an arteriovenous aneurism, is betrayed by the abrupt onset of urgent 
dyspnea, extreme engorgement of the cervical veins, and cyanosis 
and edema of the face and neck. These signs persist, should the 
subject live, and later the chest and upper extremities are disfigured 
by a maze of distended veins, while at the aortic area a vibratory 
systolic thrill, pulsation, and a variable murmur (systolic, double, 
or continuous) may develop. Rupture into the pulmonary artery, 
which is unlikely to prove so rapidly fatal as the accident just men- 
tioned, causes a continuous roaring, vibratory bruit, accentuated 
during systole, most intense over the pulmonic area, and occasionally 
accompanied by a vibratory thrill, but not by pulsation. Preceding 
the appearance of this group of signs, the patient is suddenly attacked 
by an alarming paroxysm of dyspnea, substernal pain, cough, and 
hemoptysis, symptomatic of the actual perforation. 

Aneurism of the innominate artery produces a pulsatile swelling 
at the right sternoclavicular articulation or in the suprasternal notch, 
with a systolic bruit over the tumor and conducted thence into the 
right, but not into the left, carotid. There may be duskiness and 
puffiness of the face, indicating pressure upon the left innominate and 
deep jugular veins; edema of the right arm, due to obstruction of 
the right subclavian vein; and dyspnea and dysphagia, in conse- 
quence of the sac's encroachment upon, and lateral dislocation 
of, the trachea and esophagus. Violent lancinating pain on the right 
side of the head, neck, and chest and down the right arm is excited 
by irritation of the cervical and brachial plexuses; hiccough and res- 
piratory arhythmia bespeak compression of the phrenic nerve; 
and pressure symptoms relating to the pupils, the larynx, and the 
vasomotor apparatus, indicate implication of the sympathetic and 
recurrent laryngeal nerves. 

If the common carotid artery be the seat of a circumscribed aneurism, 
which is very rarely the case, the dilatation usually occurs on the 
right side near the bifurcation of the vessel, at the level of the thyroid 
cartilage, where a pulsating vascular tumor forms. Should the 
thoracic portion of the artery be implicated, pressure phenomena, 
similar to those just noted and corresponding to the side affected, 
sometimes supervene, and if there be pneumogastric irritation, vomit- 
ing, cardiac disturbances, and respiratory irregularities are to be 
expected. 

Aneurism of the subclavian artery most commonly is situated in 



DISEASES OF THE CARDIOVASCULAR SYSTEM S°3 

the third division of this vessel's course on. the right side, and shows 
as a pulsating swelling in the right supraclavicular fossa, at the 
subclavian triangle. Edema, pain, numbness, and loss of power in 
the corresponding arm may occur from pressure upon the subclavian 
vein and the brachial plexus; hebetude, vertigo, disordered vision, 
and venous engorgement, from interference with the jugular return 
flow; and respiratory disturbances and hiccough, from irritation of 
the phrenic nerve. 

The systolic thrill and murmur of aortic atheroma, with the asso- 
ciated arteriosclerosis, suggest aneurism of the arch, but in the 
former condition the aortic second sound is high pitched and ringing, 
and there is no abnormal area of dulness, no systolic pulsation, and 
no diastolic shock. The differentiation of aortic stenosis and aneu- 
rism is considered under the latter lesion. (See p. 474.) 

N on-aneurismal pulsations in the suprasternal notch and alongside 
the manubrium, due to cardiac displacement, enlargement, and 
overaction, are to be distinguished from an aneurismal throb in this 
locality. (See Fig. 125, p. 329.) Dynamic pulsation of the aorta may 
be distinctly felt and perhaps seen in the suprasternal fossa, and may 
even account for a forcible impact beneath the upper sternal area. 
Pulsation of this nature is commonly met with in neurotic, anemic 
women in whom no other signs suggestive of aneurism can be discov- 
ered, and, moreover, the thoracic pulsation is generally synchronous 
with violent throbbing of the abdominal aorta. Pulmonary retraction, 
enlargement of the right heart, cardiac displacement, and dislocation 
of the aorta by a crooked spine are additional causes of pulsation in 
the aortic area, but in such instances positive evidence of aneurism 
is lacking, other distinctive physical signs are demonstrable, and the 
previous history of the patient furnishes definite information. In 
general, non-aneurismal pulsations are strictly systolic and more or 
less diffuse, while an aneurismal throb is distinctly postsystolic, and 
frequently can be circumscribed to a very limited area of the chest- 
wall. 

Aneurism may be suggested by acute aortitis, which is attended by 
retrosternal pain, dyspnea, precordial oppression, carotid throbbing, 
pulse irregularity, and, inconstantly, parasternal dulness due to aortic 
dilatation. In aortitis, however, the clinical picture develops most 
abruptly; bruit, thrill, and diastolic shock are lacking; and the blood- 
pressure of the two radials does not differ conspicuously. The aor- 
titic second sound, unlike the aneurismal, may have a peculiar val- 
vular clanging quality, termed by Potain the bruit de tabourka, from 
its resemblance to the sound of the Oriental native drum of this 



504 PHYSICAL DIAGNOSIS 

name. Inasmuch as both aortitis and aneurism are generally 
traceable to syphilis, a positive Wassermann test is not distinctive, 
but a rontgenograph may prove conclusive. 

Aortic regurgitation may produce pulsation of the aorta, and 
impaired resonance at the sternal end of the second right interspace, 
due to moderate dilatation of the ascending arch. But in pure 
Corrigan's disease all the accessible arteries are found to beat tumul- 
tuously, an ox-heart is datected, a water-hammer pulse is common, 
and a characteristic diastolic bruit, with suppression of the aortic 
second sound, is audible. Though the coexistence of aneurism and 
aortic regurgitation may be suspected, it is impossible to identify 
the former, save by the x-rays, unless cardinal signs and pressure 
symptoms are observed. 

Empyema necessitatis resembles aneurism in that a pulsating 
tumor upon the chest-wall is common to both conditions. The site 
of an empyematous swelling is generally below and outside that of 
an aneurismal tumor, definite signs of fluid in the left pleura are 
found, thrill, diastolic shock, and expansile pulsation are wanting, 
and exploratory puncture shows pus. (See Fig. 125, p. 329.) 

Cervical rib, by pressure upon the subclavian artery, may ac- 
count for several significant aneurismal signs in the supraclavicular 
space — dull pulsating tumor, thrill, systolic murmur, and difference 
in the radial pulses, but in an instance of this sort the #-ray gives 
accurate evidence as to the real factor of the puzzling signs. In 
some cases of this sort the anomalous rib in time may actually 
produce fusiform dilatation of the blood-vessel. 

Pulmonary tuberculosis must be distinguished from so-called 
"aneurismal phthisis," in which cough, dyspnea, hemoptysis, foul 
sputum, and other evidence of bronchial catarrh, bronchiectasis, 
and pulmonary infection predominate. Compression of a bronchial 
tube by a deep-seated aneurism springing from the posterior wall 
of the arch may account for such a symptom-group, the non-tuber- 
culous nature of which is to be inferred if the sputum be habitually 
free from tubercle bacilli, if the ophthalmo-reaction be negative, 
and if there be no wasting or other constitutional symptoms of 
phthisis. In a case of this sort radioscopy may effectually settle 
the diagnosis. 

Enlargement of the thymus gland may account for parasternal 
dulness in the first and second interspaces, especially on the left 
side, but dulness from this cause, unlike that of an aneurism, 
changes to resonance when the subject, heretofore sitting with 
the chin depressed, retracts the head to the fullest extent, thus 



DISEASES OF THE CARDIOVASCULAR SYSTEM 



505 



forcing the pulmonary margins upward over the gland (T. R. 
Boggs). 

The differentiation of aneurism from mediastinal neoplasm, 
adenitis, and abscess is considered in another section. (See p. 314.) 

ANEURISM OF THE ABDOMINAL AORTA 

The abdominal aorta, being the target of a comparatively feeble 
impact by the blood column, is less commonly the seat of aneurism 
than the aortic arch. Although sometimes formed by the posterior 
or lateral wall, the sac usually springs from the anterior aspect of the 
aorta immediately below the diaphragm, in the region of the celiac 
axis, which is not infrequently also implicated; less commonly the 
dilatation is of the fusiform variety. The aneurismal tumor, as it 
enlarges, encroaches forward into the epigastrium and the left 
hypochondrium, upward beneath the diaphragm, backward against 
the spine, which may in consequence be eroded, and perhaps laterally 
as far even as the left flank. Barring those extraordinarily rare 
examples of spontaneous clotting, the sac, as a rule, bursts into the 
retroperitoneum, peritoneum, pleura, or intestine, while an arterio- 
venous communication with the inferior vena cava is a possible con- 
sequence. Some patients die of perforation or of gangrene-peritonitis, 
secondary to embolism of the superior mesenteric artery. 

The physical signs of an accessible aneurism of the abdominal 
aorta are usually clear and well defined. Inspection shows forcible 
systolic pulsation in the epigastric area, where palpation detects a dis- 
tinct tumor having a typically expansile pulsation and systolic thrill. 
On percussion it is sometimes possible to distinguish considerable 
impairment of abdominal tympany in the direction of the left epigas- 
trium, and auscultation affords a systolic, if not a double, murmur 
over the site of the swelling. The pulse in the femoral arteries is 
likely to be unnaturally delayed and diminutive. Important pressure 
symptoms may arise, affecting, according to circumstances, the spine 
(vertebral and lumbar pain, paresthesia, paralysis); the diaphragm 
(dyspnea) ; the vagus (paroxysmal vomiting) ; the inferior vena cava 
(edema of the lower extremities; ascites); the esophagus and gut 
(dysphagia; intestinal obstruction); and the ureters and common 
bile-duct (renal and biliary colic) . 

The diagnosis of an abdominal aneurism is easily made when an 
expansile tumor can be felt beneath the belly-wall, this expanding 
property of the pulsation being radically different from the lifting 
throb of a normal aorta communicated to the surface by an over- 
lying mass of feces or by an abdominal neoplasm; moreover, as 



506 



PHYSICAL DIAGNOSIS 



Osier insists, a solid tumor (i. e., of the pylorus, pancreas, or 
liver) usually falls forward away from the aorta, and hence ceases 
to pulsate when the patient assumes the knee-chest posture, while 
an aneurismal pulsation is unaffected by this maneuver. The 
epigastric throbbing of a pulsating ventral aorta, ordinarily occurring 
in neurotic, anemic females, is never truly expansile, though when 
pressed upon, the vessel may generate a thrill and murmur. 



SECTION VII 

EXAMINATION OF THE ABDOMEN AND THE 
ABDOMINAL VISCERA 



CLINICAL ANATOMY 

Upon the surface the abdomen extends from the subcostal angle 
and costal arch to the pubic crest and folds of the groin, being 
bounded lateroposteriorly by the iliac crests, flanks, lower ribs, loins, 
and vertebral column. Internally, the abdominal cavity reaches 
from the diaphragm above to the pelvic outlet below. The shape 
of the abdomen varies greatly according to individual differences 
determined by age, sex, muscular development, and the amount of 
subcutaneous and omental fat; in general, it conforms to the out- 
line of an ovoid bulged centrally, flattened anteroposteriorly, and 
longest vertically. Normally, the contour should follow a moderate 
convexity the gentle curve of which is exaggerated in either flank, 
and shows various linear depressions and local elevations correspond- 
ing to the anatomic structures of the parietes. In the average adult, 
however, this ideal is seldom realized, thanks to the deforming influ- 
ences of corsets, childbearing, and sedentary habits. In a man 
under forty years of age the abdominal circumference at the navel 
should be from 2 to 4 inches (5 to 10 cm.) less than the thoracic 
circumference at the nipple, but during the next decade these two 
measurements tend to become equalized, until, at fifty, the girth of 
the average man's belly is as large as, if not larger than, that of his 
chest. (Cf. p. 72.) In a woman the maximum width of the abdomen 
is at a lower level than in a man, and the female waist line, as fixed by 
dressmakers' tradition, should be about 10 inches (25 cm.) less than 
the bust measurement. In a child the greatest abdominal width is 
in the upper flanks, and the belly, as a whole, is relatively large, 
owing to the disproportionate volume of the liver and to the small 
size of the pelvis, whereby the intestines and bladder are crowded 
upward. 

As anatomic landmarks, useful in the physical examination of 

507 



5 o8 



PHYSICAL DIAGNOSIS 



the abdomen, there is available a number of parietal markings upon 
the base of the thorax and the belly musculature, while, in suitable 
instances, one is also guided by certain arbitrary points fixed upon 
the anterior abdominal wall with relation to underlying viscera (Fig. 
192; cf. Fig. 21). The upper abdominal region presents two well- 
defined surface markings: the epigastric hollow of the scrobiculus 
cordis, or the pit of the stomach, which lies directly below the sub- 
costal angle and is bounded laterally by the inner borders of the 
seventh costal cartilages; and the costal arch, diverging on either side 




! Scrobiculus cordis (in- 

~" r ■- frasternal depression) 

Linea alba — : §-- 

Tenth costal cartilage v~ - T . 

to M~\, _„_--" Lines transversae 

Linea semilunaris; - ( -"'"' 

__j^ Anterior superior iliac 

spine 

Symphysis pubis —- - — .— x ~ Poupart's ligament 

Fig. 192- — Normal abdominal landmarks. 

from the apex of the subcostal angle and extending thence downward 
to its base formed by the tenth costal cartilage. By thrusting the 
finger-tips inward between this point and the iliac crest the free 
extremities of the eleventh and twelfth ribs can be palpated. The 
important bony landmarks of the lower abdomen are the pubic 
symphysis and the anterior superior iliac spines, with relation to 
which it is convenient to orient lesions of the lower abdominal zone. 
On either side of the symphysis lie the pubic spines, whence the 
inguinal ligaments of Poupart run upward to the anterior superior 
spines of the ilia. The most conspicuous anatomic point upon 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 509 

the belly wall is the umbilicus, or navel, which, normally, lies in 
the middle line at about the level of the highest part of the iliac crests 
and opposite the body of the fourth lumbar vertebra. Like the 
nipple, the navel has a most variable site: it is considerably lower in 
children than in adults, and, naturally, shifts its position when the 
abdomen is overfat, wasted, distended, or pendulous (v. i.). The 
linea alba, or the vertical tendinous white line between the recti 
muscles, runs from the tip of the xiphoid process to the pubic sym- 
physis, and can usually be identified as a narrow median furrow 
above the umbilicus, below which point its course, if perceptible at 
all, is indicated by a linear deposition of pigment {linea nigra), or, in 
men, by a matted line of converging hairs. In a well-muscled man 
two or three linece transversa of the rectus abdominis are visible 
as horizontal furrows, at the level of the seventh costal cartilage, 
at the base of the costal arch, and just below the umbilicus. 
The linece semilunares, corresponding to the outer borders of the 
recti, extend downward, with a moderate outward curve, from the 
ninth costal cartilage to a point midway between the umbilicus and 
the anterior superior iliac spine, and thence to the pubic spine. In 
the obese abdomen horizontal cutaneous flexion-folds are frequently 
visible, one at the level of the umbilicus and another about an inch 
(2.5 cm.) above the pubes. The lateral walls of the abdomen 
between the thorax and the ileum form the flanks, which, lacking 
rigid osseous and muscular support, commonly form a moderate 
local bulging below the costal arch. Posteriorly, the abdomen is 
supported by the pelvic walls, the lower ribs, and the spinal column, 
whose median furrow extends downward to the sacral triangle or the 
shallow depression overlying the sacrum. The region of the loin 
includes that part of the back between the twelfth rib and the iliac 
crest. 

The course of the abdominal aorta is indicated by a line directly 
to the left of the linea alba drawn from the ensiform to the level of 
the highest part of the iliac crest. At this level (j inch, or 19 mm. 
below the navel) the aorta divides into the two common iliac arteries 
which diverge toward a point midway between the anterior superior 
iliac spine and the pubic symphysis. The celiac axis corresponds 
to a point on the aortic line about 4 or 5 inches (10 or 12.5 cm.) 
above the navel, and between these two levels, from above down- 
ward, lie the superior mesenteric artery, the renal arteries, and the 
inferior mesenteric artery. The deep epigastric artery follows a line 
extending from the umbilicus to the middle of Poupart's ligament. 
The inferior vena cava, lying to the right of the aorta, virtually 



5 IQ 



PHYSICAL DIAGNOSIS 



follows the surface markings of this vessel, its left common iliac 
branch being crossed by the right common iliac artery just below 
the aortic bifurcation. 



TOPOGRAPHIC LINES AND AREAS 

As an aid in determining the exact position of the abdominal 
organs and the lesions thereof the surface of the abdomen may be 
divided by two vertical and two horizontal lines into seven definite 
areas 1 (Fig. 193). The two vertical 01 Poupart's lines are indicated 



Poupart's vertical 



1 1 1 

1 [ 1 «. 

i ' ' ' '4 

' ! ' 

! S 

4 ^L^. 



"^Infracostal 



Interspinal 



Fig. 193. — Topographic lines of the abdomen. 

by the downward continuation of the right and left midclavicu- 
lar lines, and extend perpendicularly from the tip of the ninth costal 
cartilage to a point on Poupart's ligament midway between the 
anterior superior iliac spine and the pubic symphysis. Of the two 
horizontal lines, the upper one, or the infracostal, joins the lower 
borders of the tenth costal cartilages and passes backward to meet 
the line of the twelfth thoracic vertebra at the posterior axillary 
line. The lower horizontal line, or the interspinal, connects the two 

1 The two abdominothoracic regions (hypochondriac or inframammary) are 
described in connection with Topographic Areas of the Thorax, on page 79. 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 511 



anterior superior iliac spines and runs posteriorly to the vertebral 
column along the iliac crests. (See p. 79.) 

The topographic areas (Fig. 194), delimited by the foregoing lines, 
are designated, from above downward, on the anterolateral aspects 
of the belly as follows : 

The epigastric region, lying between the borders of the costal 
arch and the infracostal line, overlies the liver, gall-bladder, stomach, 
duodenum, pancreas, and kid- 
neys. 

The umbilical region, or 
the central rectangular area 
formed by the crossing of the 
horizontal and the vertical 
lines on the anterior abdom- 
inal wall. Beneath this sur- 
face area lie the transverse 
colon, small intestine, mesen- 
tery, greater omentum, and 
kidneys. 

The hypogastric or pubic 
region, extending from the 
interspinal line to the pubic 
bone and bounded laterally 
by Poupart's lines. The 
hypogastrium corresponds to 
the coils of the ileum, the 
sigmoid flexure, the cecum 
(and frequently the appen- 
dix), the gravid uterus, and 
the normal bladder in the 
child, or the distended blad- 
der in the adult. 

The lumbar region, on either side of the umbilical area and 
between the infracostal and interspinal lines, the posterior con- 
tinuations of which it lies between from Poupart's line to the 
spinal column. In the right lumbar region are the ascending 
colon, ileum, and right kidney, and in the left, the descending 
colon, jejunum, and left kidney. 

The iliac or inguinal region, consisting of a triangular area in each 
groin bounded by Poupart's ligament, Poupart's line, and the inter- 
spinal line. The cecum, vermiform appendix, and ileum occupy 
this region on the right side, and the sigmoid colon, ileum, and jeju- 
num, on the left. 




Fig. 194. 



-Topographic regions of the ab- 
domen. 



512 PHYSICAL DIAGNOSIS 

METHODS OF ABDOMINAL EXAMINATION 

All four of the cardinal methods of physical diagnosis are applicable 
to the examination of the abdomen, according to the exigencies of 
the individual case, but in routine work inspection and palpation 
are chiefly relied upon, percussion being mainly a confirmatory 
step, and auscultation being resorted to only in exceptional instances. 
Mensuration is commonly used in connection with these procedures, 
to fix the exact position of pathologic signs, and to ascertain 
abdominal circumferences and surface distances. As already pointed 
out, the aspirating needle is sometimes indispensable in dealing with 
abdominal lesions, and occasionally this is also true of the x-ray. 

The general principles of the preceding steps will be outlined 
below, and their special application under both normal and pathologic 
circumstances considered in connection with the examination of 
the different abdominal organs. (See p. 531 et seq.) 

For a general examination of the abdomen, which should be bare 
from epigastrium to pubes, the dorsal decubitus is ordinarily chosen, 
the subject lying upon the back in an unconstrained, symmetric 
posture, with the knees drawn up and the shoulders elevated by a 
pillow, and breathing deeply with the mouth wide open. Attention 
to these details favors relaxation of the musculature, so essential for 
dependable results from visual and tactile examination. Stubborn 
rigidity of the belly wall, the bane of successful palpation, ma> have 
to be overcome by anesthesia or by the somewhat impracticable, 
though efficacious, expedient of immersing the patient in a warm 
bath. Small talk, to divert the patient's attention, will, however, 
generally induce sufficient muscular relaxation to allow a satisfactory 
examination. 

The erect position is indicated in the investigation of certain types 
of abdominal enlargement and anomalies of contour, due, for example, 
to visceral prolapse, to tumor, or to sagging of the parietes. Lateral 
decubitus upon the unaffected side is useful in searching for unilateral 
enlargements, as of the liver and the spleen, and in comparing 
the postural changes of the percussion sound elicited with the 
patient in dorsal recumbency, as in intra-abdominal accumulations 
of fluid. The knee-chest posture is employed when attempting to 
palpate small abdominal masses and in testing the effect of gravity 
upon a pulsating tumor, which, if aneurismal, continues to heave 
despite the subject's genupectoral attitude, whereas, if the pulsation 
be transmitted from the aorta to an overlying tumor, it ceases when 
the pressure upon the vessel is relieved by this maneuver. 

Inspection shows the size and configuration of the abdomen, the 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 513 

condition of the skin and subcutaneous structures, and the character 
of various movements visible upon the surface. By this method of 
inquiry, then, the following details are investigated: deviations from 
the normal contour of the belly relating to its general enlargement or 
retraction and to local prominences; the color and nutrition of the 
skin and the presence or absence of edema, eruptions, scars, dilated 
veins, enlarged glands, and other subcutaneous nodules; and the 
movements of the parietes due to respiration, peristalsis, and cardio- 
vascular pulsation. Perfect symmetry of posture is necessary, in order 
to recognize slight deviations from the normal contour of the abdo- 
men, which should be inspected from several viewpoints — anterior, 
oblique, and lateroposterior — according to the requirements of the 
examination. The light should fall obliquely, not perpendicularly, 
upon the surface, so as to exaggerate trifling peculiarities of form 
and of movement. 

Palpation not only confirms many of the signs obtained visually, 
but also is the means of investigating the sensitiveness of a part 
and the tension of the abdominal wall; of detecting tumors and fixing 
their site, mobility, and consistence; and of recognizing fluctuation, 
pulsation, thrills, and friction-rubs. An educated sense of touch is 
as important in studying abdominal lesions as is a trained ear in 
interpreting cardiac and pulmonary sounds. Muscular relaxation 
having been secured, the palpating hand is gently laid, palm down- 
ward, upon the surface of the abdomen, and, with firm but gentle 
pressure, the general contour of the underlying structures is deter- 
mined. Taking advantage of the phases of expiration, when the 
abdominal wall is relaxed, a deep and sliding method of palpa- 
tion, from right to left and from above downward, frequently 
enables one to outline with fair accuracy the stomach and the 
large intestine, if undue force is not used. Should a point of 
resistance be found, its shape, motility, and density are ascer- 
tained by deeper pressure with the fingers, still keeping the palm 
of the hand close to the surface and avoiding abrupt pressure with 
the finger-tips. This only tickles the patient and excites a local 
spasm of board-like rigidity. It may be added that a cold hand 
placed upon the belly will chill it into a similar contraction. The 
entire surface of the abdomen is covered in the manner described, 
the hand traveling consecutively over the different areas, the con- 
tents of which are meanwhile rehearsed by the examiner. Nervous- 
ness of the patient, abdominal tenderness, and fat, muscular, or 
edematous parietes are the principal difficulties that interfere with 
one's tactile appreciation. When the organs are not palpable because 
of ascites, it is well to try "dipping," which consists of a series of 
33 



514 PHYSICAL DIAGNOSIS 

sudden deep downward thrusts with the finger-tips over the enlarge- 
ment sought for. This manipulation momentarily displaces the fluid 
overlying the obscure viscus or tumor so that it may be felt plainly. 

Bimanual palpation of the abdomen is performed with the patient 
in dorsal decubitus, the examiner being seated by the bedside and 
palpating the anterolateral surface of the belly with one hand, while, 
with the other hand applied posteriorly, firm upward pressure is 
made against the relaxed structures of the loin and flank of the 
corresponding side. This procedure, aside from facilitating the 
palpation of fixed viscera like the liver and the spleen, is also useful 
in the tactile examination of movable solid bodies within the abdomi- 
nal cavity — tumors, enlarged glands, and movable kidneys. In out- 
lining solid intra-abdominal masses H. A. Kelly practises " bimanual 
vibratory palpation," which consists of making a succession of rapid 
tremulous movements with the palpating fingers over the surface of 
the mass, whereby these tactile impressions are conducted to the 
underlying hand. 

Mensuration is a valuable adjunct to the foregoing methods, in 
that comparative measurements of the abdominal circumference and 
of various surface distances indicate the progressive changes in the 
size of the belly that attended, for example, ascites, leukemic spleno- 
megaly, and large neoplasms. The abdominal girth is usually meas- 
ured at the level of the umbilicus, and from this point it is also con- 
venient to compute mural distances, upward to the tip of the xiphoid, 
downward to the pubic symphysis, and obliquely to the anterior 
superior iliac spines. 

Percussion of the abdomen is resorted to principally as a means 
of confirming the data obtained by inspection and palpation, in com- 
parison with which percussion, as an individual method of inquiry, 
is of distinctly inferior value. According to the technic and principles 
elsewhere described (p. 12 et seq), abdominal percussion is employed 
chiefly in delimiting the boundaries of the liver and the spleen, in 
detecting overdistention of the bladder, and in corroborating the 
visual evidences of meteorism and of fluid within the peritoneal 
cavity. Forced inspiration on the part of the patient, which de- 
presses the viscera and approximates them to the abdominal wall, 
aids the judgment of percussion signs. 

The normal tympany of the abdomen varies in intensity, pitch, 
and duration with the volume and pressure of air in the viscus per- 
cussed. If no disproportionate distention exists, the stomach 
emits louder, lower-pitched, and better sustained tympany than the 
intestines, and the same is true of the tympany afforded by the large 
gut in comparison with that of the small. Abdominal tympany is 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 5 1 5 

exaggerated by meteorism, and variously impaired by factors such 
as emptiness and collapse of the bowels or by fecal masses therein, 
distention of the urinary bladder, fluid effusions, neoplasms, and 
enlargements of the various abdominal organs. Auscultatory per- 
cussion affords, in skilled hands, an accurate method of outlining the 
stomach, of discovering abnormalities in the size and position of 
the gut, and of localizing intra-abdominal tumors. 

Auscultation is generally dispensed with in a routine examination 
of the abdomen, since its usefulness is limited to special conditions. 
The sounds audible over the abdomen are chiefly intestinal and gastric, 
less commonly frictional, and rarely of cardiovascular origin. The 
normal intestines are the seat of a medley of liquid gurgles and 
sonorous and sibilant cooing sounds caused by the rush of gas 
through the unequal lumen of the gut. Should the latter be 
stenosed such sounds are greatly intensified, provided that intestinal 
peristalsis persists. Over the stomach the transmitted heart and 
voice sounds are sometimes heard as hollow metallic echoes, and 
here also the bubbling and splashing of fluid within the stomach 
may be detected. In gastric dilatation and in fermentive gastritis 
these noises are exaggerated and intermingled with a curious sort of 
seething effervescence. The various kinds of friction are more often 
to be recognized by auscultation than by tactile sense. Peritoneal 
friction, which does not differ acoustically from the pleural rub, is 
generally excited only by respiration, although, rarely, active peristal- 
sis of the gut is the exciting factor of the sound. The sounds of 
tubercle friction and of gall-stone crepitus possess a harsh crunching 
quality and are best elicited by combined auscultation and pal- 
pation. In infants and young children the respiratory sounds, as 
well as pulmonary and pleural adventitious sounds, are distinctly 
audible over the abdomen (H. L. K. Shaw). The abdominal aus- 
cultatory signs of cardiovascular origin include the fetal heart sounds 
and the uterine souffle of pregnancy; the murmurs of hepatic cir- 
rhosis and of splenomegaly; the bruits of aneurism and of compres- 
sion of the abdominal aorta; and the hollow echo of a heart murmur 
transmitted downward and amplified by an air-filled viscus and by 
the telephonic properties of the parietes. 

CLINICAL TYPES OF ABDOMEN 

Several intra-abdominal affections account for conspicuous 
deviations from the normal size and shape of the abdomen, as in 
ascites, visceral ptosis, intestinal or peritoneal meteorism, and states 
of extreme inanition, in all of which the abnormal configu- 



5i6 



PHYSICAL DIAGNOSIS 



ration of the belly may present a most distinctive clinical picture. 
Abdominal enlargements belonging to this group are to be distin- 
guished from those symptomatic of obesity and of pregnancy, which, 
for the sake of comparison, will be considered in connection with 
these pathologic types. 

The Obese Abdomen. — In abdominal enlargement due to this 
very common cause the subcutaneous deposition of fat can be easily 
identified by rolling a fold of the skin between the fingers. Ordinarily 

the belly protrudes as a sym- 
metric globular enlargement 
which depresses the navel, ac- 
centuates the cutaneous flex- 
ion-folds, arches the pit of the 
stomach, and encroaches upon 
the flanks and the pubes; or, 
should the musculature be 
relaxed and flabby, the ab- 
domen may be pendulous, 
creased by deep transverse 
furrows, and lobulated by ir- 
regular islands of fat (Fig. 

195)- 
The Scaphoid Abdomen. 

— The scaphoid abdomen, or 
boat-shaped belly, typifies the 
extreme stage of abdominal 
retraction and wasting conse- 
quent to intestinal emptiness 
and contraction, to disappear- 
ance of the panniculus adi- 
posus, and to tonic spasm of 
the parietal musculature. In 
the typical instance the ab- 
domen is sunken or hollowed 
out like a basin or a boat, whose sides closely correspond 
to the concavity of the bony pelvis. The flanks are deeply 
indented, the costal margins converge and thus narrow the sub- 
costal angle, the xiphoid and Poupart's ligaments stand out con- 
spicously, and the iliac crests rise high above the surface of the 
sunken belly. The abdominal viscera and other structures are 
palpable as distinctly as if the subject were an anatomic model, 
and the area of normal abdominal tympany is greatly restricted, 
while pulmonary resonance usually extends below its normal limit. 







Fig. 195. — The obese, relaxed abdomen (Jef- 
ferson Hospital). 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 517 

Extraordinary bodily wasting commonly attends these abdominal 
changes, and to such extremes may the general emaciation progress 







Fig. 196. — The scaphoid abdomen (Philadelphia General H 



h 



ospit 



that the patient, as the accompanying picture testifies, literally may 
become a living skeleton (Fig. 196). The scaphoid abdomen is met 
with in its typical form in tuberculous meningitis, in chronic perito- 
nitis, and in states of inanition inci- 
dent to prolonged vomiting, chronic 
diarrhea, and stricture of the gullet or 
the pylorus. It has been observed also 
in simple meningitis, in cerebral tumor, 
and in the colic of plumbism. 

The Abdomen of Pregnancy. — 
Flattening of the hypogastrium, appre- 
ciable by or before the third month 
after conception, is the earliest visible 
change in the abdominal contour caused 
by a gravid uterus. By the fourth 
month this gives way to suprapubic 
fulness, which progressively increases 
and extends upward at the rate of 
about } inch (1.9 cm.) each fortnight, 
until by the sixth month the swelling 
reaches the level of the umbilicus, and 
by the eighth month, the xiphoid. 
During the later months of gestation 
the abdomen presents a general enlarge- Fig. 197.— The abdomen of preg- 

. . . . . . nancy (Jefferson Hospital). 

ment, which, from an anterior aspect, 

with the subject erect, is of roughly pyriform shape, with the tapered 
end below, while the profile of the belly shows a symmetric protu- 
berance more marked anteroposteriorly than laterally (Fig. 197). 
Primarily, the enlargement extends upward in the median line, but 
later a slight dextral deflection is commonly noted, and the shape is 
but slightly altered by postural changes. The flanks are uniformly 




5i8 



PHYSICAL DIAGNOSIS 



rounded, the subcostal angle is moderately widened, and the navel, 
at first depressed, gradually rises to the surface, and finally pouts 
prominently. These changes, observed in primiparae with firm 
abdominal walls, are naturally subject to modifications of contour 
in women whose parietes have been unduly stretched by previous 
childbirth or by visceral ptosis, under which circumstances anterior 
bulging and sagging of the dependent part of the abdomen are 
especially conspicuous. Of the numerous associated objective 
evidences of pregnancy, those of special interest to the clinician include 
the fetal cardiac sounds, the uterine bruit, abdominal ballottement, 
a palpable fetal outline, mammary changes, 
^rffel ' stria? gravidarum, and overfulness of the 
{fL^ B superficial veins. 

• **■ ^ e Ascitic Abdomen. — Alterations in 

Jm the appearance of the abdomen due to 

ascites, or dropsy of the peritoneal cavity, 
vary with the volume of the contained fluid 
and the pressure thereby produced. If the 
effusion be moderate, nothing more definite 
is perceptible than slight bulging of the 
flanks with flattening of the belly's summit, 
in the dorsal posture, with unnatural ful- 
ness of the lower abdomen when the patient 
stands erect. The dependent parts afford 
a dull or a flat percussion sound which 
shifts with change of posture and conse- 
quent gravitation of the fluid and ascent 
of the buoyant intestines. With the sub- 
ject in dorsal decubitus, the flanks are flat 
(fluid) and the summit of the abdomen is 
tympanitic (gut), but when the patient turns 
upon the side the opposite flank, origin- 
ally flat, will become tympanitic as the intestines float upward upon 
the surface of the gravitated fluid and lie directly beneath the pari- 
etes under the examiner's pleximeter finger. In the knee-chest 
posture both flanks give tympany, while the central part of the 
abdomen is flat. These percussion changes, it must be understood, 
may not be perceptible in a small effusion (of less than 50 ounces, 
or 1500 cc), nor when it is so large as to prevent contact between 
the gut and the parietes. 

If the effusion be of large volume there is a proportionately strik- 
ing enlargement of the abdomen, in the form of a smooth, tense, uni- 
form globular protuberance which curves downward from the 




7am 

Fig. 198. — The ascitic abdo 
men (Jefferson Hospital). 



€; 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 519 

epigastrium, fills the flanks, overhangs the hypogastrium, and oblit- 
erates the umbilical fossa, if, indeed, the navel does not actually 
protrude from the surface (Fig. 198). The shape of the abdomen 
distended to such a degree is slightly, if at all, affected by postural 
changes, and, provided that the mural tension be not excessive, the 
fluid will give a distinctive wave of fluctuation, recognizable commonly 
by the eye as well as by the palpating hand. (See p. 528.) A 
pendulous abdomen full of free fluid bulges particularly toward the 
middle line, so as to produce a disproportionately elongated protu- 
berance having a broad, sagging base, the shape of which visibly alters 
when the subject changes from the erect to the recumbent position. 
The abdominal cavity alone may be dropsical, as is generally the 
case in hepatic cirrhosis, in tuberculous peritonitis, and in Pick's dis- 
ease; or the ascites may be part and 
parcel of an anasarca of cardiorenal 
origin, in which event the edema also 
invades the abdominal wall to a greater 
or less extent. 

The Gaseous Abdomen. — The dis- 
tention symptomatic of tympanites or 
meteorism may be most extraordinary, , J 

the abdomen becoming symmetrically 
ballooned in the form of a tense tym- 
panitic sphere which preserves the same 
contour irrespective of postural change, 
and whose pressure upon the dia- 
phragm embarrasses the respiratory 
movements and disorders the cardiac 
action (Fig. 199; cf. Fig. 211). A veri- 
table " wind bomb " in the belly is the 
apt description of this condition found 
in one of Ben Tonson's plays. The * _, ' . 

J r J Fig. 199. — The gaseous abdomen 

abdominal walls are universally taut, (Jefferson Hospital), 

smooth, and shiny, the umbilicus is on 

a level with the surface or protrudes above it, and in the extreme 
case the lower part of the bony thorax projects anterolaterally. 
In gastro-intestinal meteorism it is sometimes possible to distin- 
guish the contour and the peristaltic movements of the gaseous 
stomach and gut, but in meteorism due to the accumulation of gas 
within the peritoneal cavity the abdomen is uniformly enlarged and 
neither the outline of the gastro-intestinal tube nor any movement 
thereof is perceptible. (See p. 545-) The tympany of intestinal 
meteorism encroaches upon, displaces, and perhaps obliterates the 



/ 



520 



PHYSICAL DIAGNOSIS 



areas of hepatic and splenic flatness. In pneumoperitoneum the 
property of the intraperitoneal free gas to seek the highest level 
may afford a most distinctive alteration of the percussion sound 
when the patient turns from dorsal to left lateral decubitus. In 
the dorsal posture, despite the replacement of hepatic flatness by 
tympany anteriorly, dulness persists laterally in the right axillary 
region, but if the subject turns upon the left side this axillary dul- 
ness at once changes to tympany, inasmuch as the free gas rises to 
fill the space beneath the parietes created by the gravitation of the 
liver toward the dependent side. 

Unfortunately, this changeable dulness in the axilla is not always 
demonstrable, for hepatic dulness may be wholly obliterated by a 

greatly distended colon. In such in- 
stances, then, the only certain means 
of differentiating pneumoperitoneum 
and intestinal meteorism is an ex- 
ploratory puncture of the peritoneal 
cavity. (Seep. 58.) 

The Gastroptotic Abdomen. — 
When the subject stands erect, gas- 
troptosis, or downward displacement 
of the stomach, produces a bulging 
that appears most conspicuous in the 
umbilical region, with deepening of the 
epigastrium, leveling of the umbilical 
depression, and a variable degree, of 
flaccidity and thinning of the parietes 
(Fig. 200). In typical examples the 
abdominal contour is a fairly sym- 
metric curve from the infracostal 
line to the pubes, the flanks are flat 
or even hollow, and each groin is 
seamed by a deep furrow paralleled 
above by a local saugage-shaped bulg- 
ing of the belly wall. When gastrec- 
tasis, or dilatation of the stomach, coexists, as it usually does, the 
epigastric hollow is generally effaced rather than deepened, and 
unnatural fulness at the inner borders of the lumbar regions is also 
noticeable. 

The Enteroptotic Abdomen. — Enteroptosis, or downward 
displacement of the intestines, is almost invariably associated with 
descent of the stomach and of other abdominal viscera, of which acci- 
dents, generically designated as Glenard's disease, relaxation of the 




Fig. 200. — The gastroptotic ab 
domen (Jefferson Hospital). 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 52 1 

mesentery, peritoneum, and parietes is the exciting cause (Fig. 201). 
In the upright posture enteroptosis produces a most characteristic 
alteration in the size and shape of the abdomen, whose enlarged 
profile may be likened to that of a gourd or of a sagging sac, while 
the anterior aspect is roughly pear shaped, with an evenly rounded 
base. The anterior abdominal wall slopes gently downward from 
the epigastrium to the navel, where it bulges in all directions into a 
huge flabby paunch, full of distended and constipated gut, hanging 
far beyond and below the pubes, and 
overlapping laterally to form deep 
cutaneous folds, often painfully ex- 
coriated, which course obliquely up- 
ward as far as the summits of the iliac 
crests. There is unnatural flattening 
of the epigastric concavity and more 
or less effacement of the umbilical de- 
pression, and the abdominal wall is 
generally wasted, stretched, and dis- 
figured by silvery striations. With 
the subject in dorsal decubitus, the out- 
lines of the stomach and intestines may 
be distinctly visible, owing to the pa- 
rietal thinning and relaxation, and in 
the extreme instance, there may be 
a hernial protrusion of the abdominal 
viscera through a separation between 
the recti abdominales. When enterop- 
tosis and obesity are combined a most 
peculiar lobulated enlargement of the p . g 20I ._ The en teroptotic ab- 

abdomen develops, characterized by a domen (Jefferson Hospital). 

remarkable globular protrusion and 

sagging at the base, and by unusual depth of the lateral cutaneous 
creases. Enteroptosis is very commonly associated with downward 
displacement and unnatural mobility of the kidneys, and, less com- 
monly, of the liver and spleen. 

LOCAL ABDOMINAL ENLARGEMENTS 

In dealing with circumscribed enlargements of the abdomen, their 
general situation, whether in an upper, lower, central, or lateral zone 
of the belly, should be determined first, and then, for the sake of 
greater accuracy, their more precise relation to one of the arbitrary 
regions lying between the costal arch and the pubes. In such local- 




522 



PHYSICAL DIAGNOSIS 



izations, however, no hard and fast lines of demarcation are possible, 
since swellings occupying one region must, by their evolution, sooner 
or later tend to encroach upon neighboring areas. For example, the 
splenomegaly and hepatic tumor of Banti's disease primarily cause 
bulging below the costal arch, but ultimately the visceral enlargements 
distend the greater part of the abdomen, extending downward to the 
umbilicus, and perhaps into the iliac fossae and pelvis. It is the 
origin of the swelling then, rather than its actual site, which is the 
important point to remember in studying a local abdominal enlarge- 
ment. 

Enlargements of the upper abdomen below the right costal arch are 
suggestive of lesions of the liver and gall-bladder — hepatoptosis, 
congestion, cirrhosis, amyloid disease, malignant and gummatous 
tumors, echinococcus cyst, and abscess of the liver; and lithiasis, 
empyema, or cancer of the gall-bladder. Or a swelling here may be 
due to a fecal or a malignant tumor of the ascending colon in the 
neighborhood of the hepatic flexure. Right-sided subphrenic pyo- 
pneumothorax may produce an immobile mass in the hepatic region 




Fig. 202. — Epigastric tumor in a case of gastric cancer (Jefferson Hospital). 

and perhaps in the epigastrium, and less commonly a distention of 
the upper right abdomen is traceable to nephroptosis, to an enlarged 
kidney, or to retroperitoneal adenitis. 

Enlargements of the epigastrium are referable chiefly to a distended 
or a dilated stomach, and to neoplasms of the pylorus, left lobe of 
the liver, pancreas, transverse colon, and omentum. Aneurism of 
the abdominal aorta is recognized as a pulsatile tumor in the median 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 523 

line of the epigastrium. To the right of this line an enlarged gall- 
bladder may be detected, and to the left, immediately above the colon, 
an effusion into the lesser peritoneal sac. Indurated masses in the 
epigastrium may prove to be retroperitoneal or mesenteric glands 
enlarged by tuberculosis, malignant disease, or pseudoleukemia. 

Enlargements below the left costal arch may indicate splenomegaly, 
Splenoptosis, gastric dilatation, or cancerous growths near the splenic 
flexure of the colon. Here also is the site of a left-sided subphrenic 
pyopneumothorax, of an effusion in the lesser peritoneum, and, occa- 
sionally, of renal tumor and nephroptosis. 

Local enlargements in either flank commonly depend upon lesions 
of the uterus and adnexa — pyosalpinx, ovarian, uterine, and ligament- 
ous tumors, and ectopic gestation; or a mass in one of the iliac areas 
may mean tuberculosis or malignant disease of the peritoneum, 
retroperitoneal growths, intussusception, renal tumor, or nephroptosis. 
A psoas abscess may bulge, fluctuate, and point in the groin either 
below or above Poupart's ligament, while an iliac abscess commonly 
appears above the outer end of this landmark. The right flank. 
at or near McBurney's point, is the common site of the pal- 
pable tumor of appendicitis, and in this region also may be found 
the tumors due to neoplasms of the cecum or ascending colon and 
to fecal impaction in these portions of the intestines. In the left 
flank similar obstructive lesions of the descending colon and sigmoid 
flexure are possible causes of a local swelling, additional factors to 
be borne in mind being splenomegaly and splenoptosis. 

In the region of the umbilicus, a distention is suggestive of gastric 
dilatation and displacement; less commonly, of enteroptosis or of 
other visceral ptoses — a displaced spleen or kidney may be more 
conspicuous near the navel than it is in the epigastrium or in the 
flanks. The umbilical region is also the site of hernia and of the 
tumors caused by tuberculous peritonitis, and by neoplasms of the 
stomach, gut, omentum, and mesentery. In this region also appears 
most conspicuously the cup-shaped roof of the dome-like abdomen 
of ruptured extra-uterine pregnancy, described by Shulman. 

Distention of the lower abdomen above the pubes, if not obviously 
a sign of pregnancy, may mean an overdistended bladder or, very 
rarely, physo- or hematometra. Additional factors of hypogastric 
swellings include the above-noted diseases of the female genital organs, 
the appendix, and the peritoneum, as well as inguinal hernia. 

On inspection massive abdominal tumors may account for an appar- 
ent general enlargement of the abdomen, but by careful palpation 
and percussion such growths are traceable to a local origin — visceral, 
peritoneal, or glandular. It is especially the ovarian cyst, the preg- 



524 PHYSICAL DIAGNOSIS 

nant or fibroid uterus, the leukemic spleen, the overfull bladder, 
and the cancerous gut and peritoneum which at first glance simulate 
a universal abdominal distention. In addition to these factors many 
others responsible for the various local enlargements mentioned else- 
where may, if exaggerated, also cause an apparent general dis- 
tention. 

In the distention due to an ovarian cyst the dome of the abdomen 
gives a dull percussion sound while the flanks on either side are tym- 
panitic, these signs persisting when the subject turns from the dorsal 
to the lateral decubitus. The same is true of the gravid uterus and 
of uterine fibroid. In differentiating these three conditions, vaginal 
examination, the cautious use of the aspirator, and the history of 
the patient are important diagnostic adjuncts. A leukemic spleen 
may be readily mapped out by palpation and by the dulness over 
the upper and sometimes the lower left abdominal region, and in 
this disease the blood count is pathognomonic. The distended 
bladder forms a dull area encircled by a tympanitic zone in the lower 
mid-abdomen, which findings, it need scarcely be noted, vanish after 
catheterization. In the cancerous intestines and peritoneum the resist- 
ant, nodular character of the growths, their asymmetric distribu- 
tion, and perhaps the presence of metastatic tumors furnish the 
important clues. 

ABDOMINAL MOVEMENTS 

The various movements of the abdomen to be noted on inspection 
relate to the respiratory excursions, to local areas of pulsation, and to 
peristalsis of the stomach and intestines. Exaggerated abdominal 
movements during respiration are generally due to some thoracic 
lesion which restricts the normal rise and fall of the diaphragm. En- 
feeblement of such movements occurs as the effect of abdominal dis- 
tention, pain, and paralysis, as, for instance, in ascites, meteorism, 
and tumors, in peritonitis, and in paralysis of the abdominal muscles. 
These causes, together with those of local pulsations in the epigastrium 
have already been considered. (See Anomalies of Respiration, p. 
97, and Abnormal Areas of Pulsation, p. 329.) Here may be men- 
tioned the rhythmic throbbing near the umbilicus, occasionally 
symptomatic of acute enteritis (Stokes) . 

Peristalsis of the stomach and gut may be visible under normal 
conditions in subjects with thin, flaccid abdominal walls, but more 
often it is a sign of marked gastric dilatation, perhaps with pyloric 
obstruction, or of stenosis of the intestine, with dilatation above the 
point of constriction. Exaggerated peristalsis also may be seen 
in overdistention of the gut associated with enteritis and with the 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 525 

functional neuroses. Kussmaul's "peristaltic unrest" is simply an 
excessive peristalsis, betrayed by volleys of gurgles and rumbles 
of flatus (borborygmi) , and chiefly affecting women whose neurotic 
temperament, tight stays, and overeating account for these embarrass- 
ing echoes. Visible peristalsis appears as a succession of undulatory 
movements travelling with a sort of worm-like motion across the 
belly — from left to right, if the peristalsis be of the stomach, and from 
right to left, if it be of the intestines. Peristalsis of the stomach is 
seen best in the epigastrium ; of the large intestine, in the epigastrium 
and in the right or left flank, according to which section of the tube, 
transverse, ascending; or descending, be affected; and of the small 
intestines, in the region of the umbilicus. In this situation a circum- 
scribed area of peristaltic gut, massed together coil upon coil, suggests 
stenosis at or near the ileocecal valve. 



THE SKIN AND SUBCUTANEOUS TISSUES 

The nutrition of the skin and structures beneath suffers decidedly 
in many wasting diseases, as examples of which may be cited tuber- 
culous peritonitis, malignant 
disease of the abdominal vis- 
cera, and Asiatic cholera. In 
such conditions, in addition to 
obvious wasting of the abdom- 
inal wall, the skin is dry, fur- 
furaceous, bloodless, and so in- 
elastic that it may be pinched 
up and molded between the 
fingers like a ball of putty. In 
advanced senility and in the 
multipara the abdominal pari- 
etes are thin, toneless, and re- 
laxed, and as the effect of long- 
continued distention the skin 
of the abdomen becomes tense, 
shiny, preternaturally dry, and 
even duskily blue in the de- 
pendent parts of the flanks. 
Increased thickness of the ab- 
dominal wall may be muscular, 
fatty, or edematous. Edema 
of this region is recognized as 




Fig. 203. — Venous engorgement of the ab- 
dominal wall (Jefferson Hospital). 



a boggy thickening which pits upon pressure like a soft apple, es- 
pecially in the flanks and loins; it is commonly part of the anasarca 



526 



PHYSICAL DIAGNOSIS 



of renal or cardiac disease, and may or may not be associated with 
ascites. Angioneurotic edema occasionally attacks the abdominal 
wall, appearing as an ephemeral local tumefaction, too tense to 
pit deeply and either blanched or of a scarlet hue. In the excep- 
tional instance diffuse purulent infiltration may account for a 
widespread edematous thickening of the abdominal parietes. 

As types of color changes in the skin of the abdomen and elsewhere 
there are to be recalled the saffron discoloration of icterus ; the blue 
mottling of cyanosis; the dark pigmentation of Addison's disease, 
peritoneal tuberculosis, argyria, and vagabondism; the dirty brown 
or yellow patches of tinea versicolor; and the coppery macular areas 
of syphilis. Multiple white, silvery, or, rarely, pigmented linear 
markings upon the abdomen may have been caused by pregnancy, 
ascites, and various causes of chronic abdominal distention; gener- 
ically, these streaks are designated as linece albicantes, or, if due to preg- 
nancy, as linece gravidarum. The appearance of a white line upon 
the skin of the abdomen (ligne blanche abdominale) after friction 
with a blunt instrument is described by Sargent as an occasional 
rinding in suprarenal insufficiency. Scars, aside from those due to 
accidents and to operations, may be the relic of a previous attack 
of syphilis, of a chancroidal bubo, or of a destructive skin dis- 
ease. Venereal infection, tuberculosis, malignant disease, and in- 
jury by a sudden, violent strain are suggested when enlarged 
glands are discovered in the groin. Small, steel-gray points of fat 
necrosis are sometimes perceptible in cases of pancreatitis, and 
hard subcutaneous nodules may develop just beneath the skin in 
sarcomatosis and in cancer of the abdominal organs. 

Enlarged and tortuous veins coursing over the abdomen are a valu- 
able sign of venous obstruction, and generally mean Laennec's cir- 
rhosis, although less commonly they result from portal vein throm- 
bosis, ascites, or pressure by neoplasms upon the superior or inferior 
vena cava. The caput Medusa of the gin-liver consists of a bunch 
of tortuous venules about the navel, and indicates portal obstruction, 
as the result of which there has been established a compensatory 
anastomosis between a para-umbilical vein and the superior epigastric 
veins (Sappey) . By making pressure upon an abnormally dilated 
abdominal vein it is possible to determine whether the obstruction 
involves the superior or the inferior vena cava ; if it be the former, the 
vein distends above the point of pressure, while if it be the latter, 
the fulness appears below the constriction. The flow within the 
enlarged veins radiating from the navel is away from this point. 

Umbilical Changes. — The condition of the navel is not only a good 
index of the thoroughness of one's personal hygiene, but a collateral 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 527 

sign of clinical moment. In an overfat abdomen the navel is retracted 
perhaps to the point of obliteration; it protrudes conspicuously in 
late pregnancy, umbilical hernia, and portal obstruction; and it is 
stretched and depressed in the abdominal fulnesses of early preg- 
nancy, ascites, and new-growths. The navel may be the seat of 
inflammation and eczema, and in congenital umbilical fistula it may 
ooze a clear serous fluid. F. P. Henry regards peri-umbilical ery- 
thema as an important diagnostic sign in tuberculous peritonitis. 
A malignant neoplasm of the liver may rigidly immobilize the 
umbilicus. 

Muscular Rigidity. — Increased resistance to pressure and actual 
spontaneous rigidity of the abdominal musculature are suggestive of 
either peritoneal irritation or inflammation. General rigidity of the 
belly wall is met with in acute general peritonitis, but a practically 
similar spasm also attends certain inflammations above the dia- 
phragm, particularly croupous pneumonia and diaphragmatic pleu- 
risy. Local muscular rigidity may point definitely to an inflamma- 
tory lesion of one of the abdominal organs — to appendicitis or to 
extensive typhoid ulceration, if it affects the right iliac region; to 
perisigmoid inflammation, if it be in the left iliac space; to chole- 
lithiasis, gastric ulcer, or pancreatitis, if it be epigastric. 

FLUCTUATION 

The palpating hand seldom appreciates any decided tactile differ- 
ences in the resistance of the gaseous and the liquid strata of an ascitic 
abdomen, but fluctuation, a certain sign of fluid, is demonstrable if 
a moderately large effusion be present. To obtain this sign the 
examiner palpates one flank and gently but sharply taps with the 
finger-tips the opposite side of the abdomen, an assistant meanwhile 
pressing firmly with his hand held edgewise in the median line, so 
as to cut off the vibrations of the abdominal wall. If fluid be present 
a distinct jog, due to a wave of liquid set in motion by the percussion, 
is felt by the palpating palm. Ascites does not invariably give this 
sign, for it may be impossible to agitate a liquid wave both in very 
slight and in very extensive dropsical accumulations. The percussion 
findings associated with this tactile sign of intraperitoneal fluid are 
described on p. 518. 

Fluctuation of an abdominal mass indicates encysted fluid. The 
sign may obviously relate also to an iliac abscess or to an abscess of the 
abdominal wall. In other instances it is attributable to a distended 
bladder; to pregnancy, normal or extra-uterine; to ovarian, tubal, 
hepatic, or renal cyst or abscess; and to general effusions in the lesser, 
and encysted effusions in the greater, peritoneum. 



528 PHYSICAL DIAGNOSIS 

TACTILE FRICTION AND THRILLS 

In tuberculous peritonitis coarse tubercle friction, due to the rubbing 
together of peritoneal tubercles, is sometimes elicited by kneading 
the abdomen with the finger tips. In other forms of peritonitis, 
especially the chronic, fine peritoneal friction is occasionally felt 
over the upper part of the abdomen. Over the liver a palpable 
friction-rub during respiration suggests perihepatitis, secondary 
to hepatic abscess or cancer, or developing by the extension of 
pleurisy or of peritonitis. Subphrenic peritonitis likewise ac- 
counts for tactile friction in this area. Rarely, inflammation of 
the peritoneal covering of the spleen causes a similar rub over the 
splenic area. Perihepatitic and perisplenitic friction are most dis- 
tinctly felt during full inspiration and disappear when adhesions 
form between the affected organs and the abdominal wall. Chole- 
lithiasis may underlie two tactile signs localized to the region of the 
gall-bladder: palpable friction with respiration, excited by local 
inflammation of the peritoneum at the gall-bladder and of the adja- 
cent hepatic peritoneal reflection (Gerhardt) ; and a grating gall-stone 
crepitus, due to friction of the calculi by palpatory manipulation. 

Xiphoid crepitation, a tactile sensation akin to that of emphyse- 
matous crackling, is described by Galvagni as an evidence of peri- 
tonitis. It is elicited by pressure over the xiphoid tip and the upper 
costal arch, and is explained by the mechanical separation of perito- 
neal adhesions, as well as by the presence of subcutaneous bullae 
created by gas-forming bacteria. 

A palpable thrill in the epigastrium, with visible throbbing of a 
tumor, giving expansile pulsation and a systolic murmur, is found in 
aneurism of the abdominal aorta. Over an accessible hydatid 
cyst the so-called hydatid thrill or fremitus can be sometimes 
detected by palpatory percussion. (See p. 138.) 

PAIN IN THE ABDOMEN 

It is important to bear in mind that abdominal tenderness and 
pain relate not only to lesions of the abdomen, but also to disorders 
elsewhere situated, notably those affecting the thoracic organs and 
the spine. The acutely painful abdomen of pneumonia and the 
excruciating gastric crises of tabes dorsalis are two striking illus- 
trations of pain reflected to the abdomen from remote regions, 
the examination of which should not be neglected in attempting to 
discover the true cause of a tender or an aching belly. Furthermore, 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 529 

diseases of the abdominal organs frequently account for pain in re- 
gions far removed therefrom, as in the shoulder pains symptomatic 
of lesions of the liver and colon, in the tender spine of gastric 
ulcer, and in the painful testicle of stone in the kidney. 

Generalized abdominal tenderness and pain usually is traceable to such 
conditions as gastro-intestinal disease, meteorism, peritonitis, irritant 
poisons, abdominal myalgia, or hysteria. Or when diffused through- 



Gall-bladder disease 
Robson's point 

4 

Intussusception 

McBurney's point 

Clado's point 

Ureteral disease 




iastric ulcer 



Morris's points 
Volvulus 



Fig. 204. — 1. Diseases of stomach, gall-bladder, duodenum, transverse colon, and 
pancreas; abdominal aneurism; pneumonia; phrenic pleurisy; pericarditis; appendicitis; 
diabetes; uremia; eclampsia. 2. Diseases of stomach, splenic colon; enteroptosis, 
nephroptosis, nephralgia. 3. Diseases of intestines, omentum, mesentery, and perito- 
neum; lead colic; abdominal arteriosclerosis. 4. Diseases of liver, hepatic colon, and 
right kidney. 5. Diseases of spleen, splenic colon, and left kidney. 6. Diseases of 
urinary bladder and pelvic organs. 



out the abdomen it may stand for the radiation of pain originating in 
one of the abdominal viscera or in some extra-abdominal structure, 
renal colic, appendicitis, dysmenorrhea, and diaphragmatic 



as m 



pleurisy, in which the pain, primarily circumscribed to the local 
lesion, secondarily spreads far beyond its original confines. Cir- 
cumscribed tenderness and pain should be investigated with refer- 
ence to its origin in, and reflection from, the organs and other struct- 
34 



530 PHYSICAL DIAGNOSIS 

ures corresponding to the several surface divisions of the abdominal 
wall, the findings thus obtained being interpreted in the light of a 
full clinical inquiry by other methods of examination (Fig. 204). 

Pain in the epigastrium ordinarily is of purely gastric origin, as in 
neuralgia, inflammation, ulcer, or cancer of the stomach, but to this 
region the pain of diseases of the gall-bladder and gall-ducts also is 
commonly referred. In cholecystitis deep tenderness may be in- 
duced at the end of full inspiration if the examiner's fingers be thrust 
upward beneath the costal arch at the outer limit of the right epi- 
gastrium — Naunyris sign. Epigastric pain may be symptomatic of 
duodenal ulcer or of an impacted transverse colon; of some pancreatic 
lesion, such as inflammation, hemorrhage, or carcinoma; of circum- 
scribed peritonitis; of aneurism of the abdominal aorta; of myalgia 
of the abdominal musculature; or of vertebral disease. It is also to 
be recalled that severe epigastric pain is a common complaint in 
infantile pneumonia, diaphragmatic pleurisy, pericarditis, and rheu- 
matic fever; and that it frequently accompanies visceroptosis and 
appendicular inflammation. Severe crises of epigastric pain are a 
well-known premonitory sign of diabetic coma, and less commonly 
accompany other intoxications, notably uremia and eclampsia. 

Pain in the umbilical region, if not traceable to some one of the 
conditions just enumerated, may be indicative of enteritis, enteralgia, 
intestinal obstruction or ulceration, lead colic, general peritonitis, 
omental carcinoma, or mesenteric cyst. Here also may be the seat 
of pain in abdominal arteriosclerosis, angina pectoris, ureteritis, 
and embolism of the superior mesenteric artery. The girdle pain 
of locomotor ataxia, myelitis, and spinal meningitis encircles the 
body, as a painful sense of constriction, in the upper part of the 
umbilical rectangle. Two diagnostic points of pain on pressure are 
also situated in this area of the abdomen: Mayo Robson's point, at 
the junction of the outer and middle third of a line drawn from the 
ninth costal cartilage to the umbilicus, where tenderness indicates 
inflammatory lesions of the gall-bladder and ducts; and Morris's point 
of tenderness in appendicitis, situated 1^ inches (3.75 cm.) from the 
navel on a line running thence to the right anterior superior iliac 
spine. Tenderness at this point and also at a corresponding point 
to the left of the navel suggests pelvic, not appendical, disease, in 
which the sensitiveness is right sided only. 

Hypogastric pain relates principally to diseases of the urinary blad- 
der, of which cystitis in particular, and also acute distention, calculus, 
tuberculosis, and neoplasm are accredited causes. In women uterine 
and ovarian disease, pelvic inflammation, and ectopic gestation are 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 53 t 

also to be reckoned with as possible factors of pain above the 
pubes and in the lateral regions bordering thereupon. Voillemier's 
point, selected as the site for puncturing a distended bladder, is 
situated in the linea alba 2\ inches (6.25 cm.) below the interspinal 
line. 

Either ileolumbar region may be the seat of maximum tenderness 
in abdominal pain due to colitis, hernia, varicocele, renal colic, 
floating kidney, or ovaritis. On the right side pain is suggestive 
particularly of intussusception, cecal impaction, enteric fever, and 
appendicitis; while left-sided pain in this area may indicate volvulus, 
sigmoid impaction, or pericolitis sinistra. McBurney's point of 
appendical pain is situated in the right iliac region i\ inches (3.75 
cm.) from the anterior superior iliac spine on a line drawn from 
this prominence to the umbilicus. Clado's point, having a similar 
significance, lies at the intersection of the right semilunar line by 
the interspinal line at the external border of the rectus abdominis 
muscle. 

Pain in the hypochondriac regions and in the loins and sacrum 
has been dealt with in Section II. (See pp. 122, 123.) 

EXAMINATION OF THE STOMACH 

Clinical Anatomy. — The stomach occupies the left hypochon- 
drium and part of the epigastrium, lying chiefly to the left of the 
median line in an almost vertical position, with the subject in the 
erect posture (Fig. 205). The old conception of the stomach's 
transverse position in the upper abdominal cavity must be revised 
by the newer truths of modern radiography, which shows radical 
differences in the topography of the organ according to the in- 
fluences of posture, degree of distention, and amount of contained 
food. When empty and contracted the stomach is represented by 
a small pyriform sac filled with gas, and situated beneath the left 
dome of the diaphragm. This communicates with a collapsed 
tubular structure whose opposed walls for the greater part conform 
to the vertical plane of the body except near the midline, where 
they run almost horizontally. When fully distended the stomach 
is comparable in shape to an elongated gourd of virtually uniform 
diameter following the vertical-oblique course above indicated. 

The cardia, or gastro-esophageal orifice, corresponds anteriorly 
to a point on the seventh left costal cartilage 1 inch (2.5 cm.) 
from the sternum, and posteriorly to the level of the ninth thoracic 
vertebra. The pylorus, or gastroduodenal opening, unlike the 



S3 2 



PHYSICAL DIAGNOSIS 



cardia, is freely movable, and is situated, when the stomach is 
empty, in the median line 3 or 4 inches (7.5 to 10 cm.) below the 
xiphisternal junction, but when the stomach is distended the 
pylorus moves 2 or 3 inches (5 to 7.5 cm.) to the right of the median 
line; posteriorly, the pylorus is opposite the first lumbar vertebra. 
The pyloric region also includes a vestibule, directed upward to the 
right of the median line, and a canal, running thence upward, back- 
ward, and toward the right to project into the duodenum. The 
Addison-Cunningham transpyloric line, crossing the belly midway 







J>^. 


1 ^ 


'•fu ' 


N£ Ml 





Fig. 205. 



-Surface topography of the stomach, when empty (inner broken outline), 
and in full distention (outer solid outline). 



between the suprasternal notch and the pubic symphysis, bisects 
the pyloric end of the stomach. The fundus, or the rounded dome 
of the stomach to the left of the cardia, lies behind and somewhat 
to the left of the heart's apex, and occupies the left vault of the 
diaphragm. The body, lying entirely to the left of the median 
line, is situated either vertically or somewhat obliquely toward 
the right, according to the position of the trunk, whether upright 
or recumbent. The lesser curvature, or the upper concave border 
of the stomach, lies in the epigastric region, deeply situated be- 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 533 

neath the lower border of the liver. In general, its course corre- 
sponds to that of the opposed wall of the empty contracted stom- 
ach. A distinct depression on the lesser curvature, the incisura 
angularis, separates the body from the pyloric portion. The 
greater curvature, or the lower convex border of the stomach, lies 
beneath the ninth costal cartilage at the left costal arch, and is 
situated at or slightly below the umbilicus in the median line of 




Fig. 205a. — Radiograph of the normal stomach in a state of complete distention. 
Cf. Figs. 206 and 207. (Plate by Dr. W. F. Manges.) 

the abdomen. In children it is generally much lower, even below 
the level of the iliac crests. 

Inspection. — Aside from the detection of peristalsis and of pul- 
sating areas in the epigastrium, previously described (p. 332, inspec- 
tion of the gastric region is useful in determining the size and the 
position of the stomach. In the thin subject it is sometimes possible 
to perceive the contour of the greater curvature and its respiratory 
rise and fall, even if the stomach be but moderately distended, and 
the outline of the lesser curvature may be visible if the organ be 



534 PHYSICAL DIAGNOSIS 

greatly depressed. In other instances it is necessary to inflate 
the stomach, either with air by means of a bulb-syringe, or with 
carbon dioxid evolved from sodium bicarbonate and tartaric acid. 1 
Artificial distention of the stomach may reveal a pyloric tumor 
otherwise invisible, while a phantom tumor due to a tightly con- 
tracted gastric musculature promptly disappears when the stomach 
is inflated. 

When a patient whose stomach is dilated and displaced stands 
erect, the epigastrium becomes distinctly concave, and the lower 
central and lateral regions of the belly bulge forward and sag down- 
ward in the form of a flaccid globular mass bounded on either flank 
by a deep sulcus running obliquely downward toward the pubis 
from the iliac crests. In the dorsal decubitis the epigastric hollow 
becomes shallower, the abdominal prominence flattens, and the 
enlargement of the flanks is more conspicuous. (C/. Figs. 200 and 
201.) 

Inasmuch as an enlarged stomach extends chiefly in a downward 
direction, the lower border is taken as a clinical index of the organ's 
size and site. A lower border well below the navel may safely be 
regarded as symptomatic of either dilatation or of displacement, for 
the differentiation of which other data are essential. In gastrec- 
tasis the pylorus is but slightly lower than its normal site below the 
right costal arch, the distance between the two curvatures of the 
stomach is greatly increased, and the lower border is depressed to 
the level of the navel or somewhat below it; while in gastroptosis 
the pylorus occupies the umbilical region, the distance between 
the stomach's curvatures is approximately normal, and the lower 

1 Mechanical inflation requires the introduction of a stomach-tube, to the 
buccal end of which is coupled a Davidson syringe, which is then manipulated 
until sufficient air has been pumped into the stomach. By this procedure the 
amount of gastric distention may be exactly controlled and the distressing 
symptoms of overinflation quickly relieved ; it is, however, objectionable in 
patients to whom the passage of the tube is a trying ordeal, if not a positive 
danger. Carbon dioxid inflation, the best method for the average case, is 
accomplished by giving the patient a dram of sodium bicarbonate dissolved in 
half a tumblerful of water, followed at once by a dram of tartaric acid sim- 
ilarly diluted. The carbonic acid gas thus evolved in the stomach quickly 
distends the organ sufficiently for a satisfactory examination. This process of 
chemical inflation has been criticized chiefly because the gas generation can- 
not be controlled, and hence may cause cardiac embarrassment as well as 
active gastric distress from the irritant effects of the effervescence. Practi- 
cally, overdistention is promptly relieved by the escape of gas through the 
cardia, whence it is disposed of by belching ; or, in an extremity, the tube may 
be passed to relieve the pressure. 

Organic cardiac disease, recent hematemesis, gastric ulcer and other factors 
that seriously weaken the gastric parietes are causes of possible danger in infla- 
tion of the stomach by either of the above methods. 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 535 

border lies far below the navel, perhaps almost as low as the pubes. 
From this it is evident that the site of the pylorus, and not simply 
the position of the lower border of the stomach, is the criterion in 
distinguishing dilatation and displacement of the organ. These 
signs, it must be added, are always to be supplemented by a deter- 
mination of the stomach's motor powers and by laboratory tests. 
The radiograph on this page (Fig. 206) well illustrates the size and 




Fig. 206. — Radiograph of a dilated and displaced stomach. Cf. Fig. 205a. (Plate by 

Dr. W. F. Manges.) 

site of a dilated and displaced stomach. The striking double 
sacculation of the hour-glass stomach may be made visible by infla- 
tion, and in this rare deformity it is possible to trace the outline of 
the deeply notched lower gastric border where a cicatricial con- 
traction divides the stomach into two separate compartments, one 
pyloric and the other cardiac, which communicate by a narrow 
opening (Fig. 207). An hour-glass stomach usually yields by 
siphonage less fluid than has been poured in through the stomach- 
tube, and, though apparently drained dry, may afford a sudden 
commingling of splashing sounds and other signs indicating the 
reappearance of fluid in the empty compartment. 



53^ 



PHYSICAL DIAGNOSIS 



X-ray examination of the stomach is most useful in determining 
the size, contour, position, and peristaltic action of the organ, and, 
with less certainty, the existence of neoplasms. The best results, 
both from radiography and from radioscopy, are obtained by using 
the rays after the stomach has been rendered opaque by the admin- 




Fig. 207. 



-Radiograph of an hour-glass stomach. 
Manges.) 



Cf. Fig. 205a. (Plate by Dr. W. F. 



istration of 1 pint (480 mils) of kefir, of mucilage of acacia, or of thin 
gruel containing about 1 ounce (3 1 gm.) of bismuth sulphate. 

Bismuth subnitrate, owing to its potential toxicity from nitrite- 
poisoning, has been generally abandoned in favor of the sulphate, 
carbonate, or oxid, all of which are harmless. 1 Within from four 

1 For radiographic examination of the alimentary canal the Royal Society 
of Medicine recommends standard test-meals of porridge and of bread and 
milk, each to be incorporated with 2 ounces (62 gm.) of barium sulphate or 
of bismuth oxychlorid. The porridge meal is prepared by adding to 7 ounces 
(247 gm.) of fine oatmeal sufficient milk to make the total bulk 10 ounces 
(310 cc), sweetening the mixture with brown sugar. The bread and milk is 
made by mixing 2 ounces (62 gm.) of soft white bread with 8 ounces (240 cc.) 
of whole or malted milk, sugar being added to taste. With each of these test- 
meals, to be given on an empty stomach, the proper quantity of bismuth or 
barium is mixed just before use. 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 537 

to six hours after the ingestion of this bismuth test-meal the nor- 
mal stomach shows no vestige of the salt, which passes through 
the ileocecal valve into the colon within from eight to ten hours 
and through the descending colon and rectum within twenty-four 
hours. Serial radiographs taken immediately after the patient 
swallows the bismuth meal and twenty-four hours thereafter, with 
exposures made at two-hour intervals during the first twelve 
hours, provide accurate and correlated data of the condition of the 
entire gastro-intestinal canal. Especially is this true of such a 
series supplemented by one or two radiographs of the colon taken 
after the injection of a suitable clyster. (See p. 547.) 

By combined radiography and fluoroscopy many cases of cancer 
and ulcer of the stomach are differentiated at an early period of their 
development', chiefly by criteria such as test-meal residue, pyloric 
patency, and irregularities of contour 

In gastric cancer this complex is sought for: antiperistalsis ; un- 
natural patency or actual obstruction of the pylorus ; large residue 
of the test-meal after six hours; fixation of the stomach as a whole; 
and irregularities of contour due to neoplastic deformity. In 
gastric ulcer it may be possible to identify the projecting shadow 
of the ulcerative mass, and also the extragastric cavity caused by 
the extension of a perforative process into neighboring tissues, 
hepatic or pancreatic. Other radiographic signs include indenta- 
tion of the gastric wall opposite to the site of the ulcer, an appre- 
ciable six-hour residue of bismuth, and suggestive defects of shape 
and motility, such as antiperistalsis, delayed pyloric patency, 
hour-glass constriction, and a "fish-hook" contour of the entire 
stomach. 

Gastrodiaphany, or transillumination of the stomach, requires 
the introduction into the stomach of a gastrodiaphane, or a soft 
rubber tube, to the lower end of which is attached a small incan- 
descent lamp, which when illuminated renders the gastric outline 
luminous when the examination is made in a dark room. The most 
satisfactory results from gastrodiaphany have been secured in cases 
of dilatation and prolapse, but, on the whole, the method is less 
dependable than examination after inflation of the stomach or by 
means of the x-ray. 

Palpation.— Palpation of the stomach corroborates the findings 
of inspection, and in addition reveals and localizes gastric pain and 
tenderness, tumors and thickening of the anterior wall, and suc- 
cussion waves within the organ; exceptionally, the friction fremitus 
of a perigastritis can also be felt. In 'studying gastric pain it is help- 



538 



PHYSICAL DIAGNOSIS 



ful to recall Riedel's law, that left-sided pain generally is due to 
disease of the stomach itself, while right-sided pain is more often a 
reflex sign referable to lesions of other abdominal viscera, the princi- 
pal exceptions to this general rule being in lesions of the pan- 
creas and of the pylorus. 

The pain of gastritis is more or less diffusely distributed, is usually 
increased by pressure and by taking food, and intermits without 
obvious reason. In uncomplicated gastralgia the pain occurs in 
neuralgic paroxysms which commonly radiate peripherally from a 
point low down in the epigastrium and are relieved both by pressure 
and by the taking of food. The pain of gastric ulcer is likely to be 
boring and scalding in character, sharply circumscribed to the situa- 
tion of the lesion, greatly aggravated by taking food and by pressure 
and relieved by vomiting; a tender point to the left of the spine, be- 
tween the tenth and twelfth thoracic vertebrae, is of considerable 
diagnostic importance (Fig. 68, p. 121). In gastric cancer there is usu- 
ally a dull, gnawing area of pain localized at the site of the growth, 
reflected toward the loins and the back, and accompanied by tender- 
ness along the six lower thoracic vertebrae; the pain of cancer is sub- 
ject to frequent periods of quiescence and to paroxysmal exacerba- 
tions of a gastralgic form. Other important gastric factors of pain 
in the region of the stomach include simple irritation of the organ, 
atonic dyspepsia, hyperchlorhydria, gastrectasis, and gastroptosis. 
It is also to be noted that pain of gastric origin may be simulated 
by pneumonia, pleurisy, pericarditis, spinal caries, Addison's disease, 
locomotor ataxia, and inflammatory lesions of neighboring abdominal 
organs. 

Tumors of the stomach are most frequently found at the pylorus, 
either at its normal site or lower down, owing to the associated changes 
in the size and position of the organ. Such tumors are generally 
carcinomatous, the pylorus being the favorite seat of this type of 
neoplasm, and may be either freely movable or firmly anchored, 
depending upon the extent to which they are bound down by adhesions. 
Neoplasms of the greater curvature may be palpable in the hypogas- 
trium or in either hypochondrium ; growths of the anterior wall are 
made more prominent and those of the posterior wall are obscured 
when the stomach is distended. Riegel emphasizes the importance 
of distinguishing a tumor of the lesser curvature from the pancreas, 
which in the subject with a thin, relaxed abdominal wall occasionally 
is palpable through the empty stomach, or above it, if the organ be 
displaced. Inflation, however, will settle such a doubt by hiding 
the pancreas and by clearly localizing a gastric tumor. Ewald points 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 539 

out that in various forms of gastritis the inflammatory swelling of a 
gastric lymph-node forms a small movable tumor at the middle of the 
greater curvature. Hypertrophic fibrosis of the pylorus, local thick- 
ening of the anterior wall, nephroptosis, fecal masses, and small 
epigastric hernias are other abdominal swellings which are to be dis- 
tinguished from tumors of the stomach itself. 

Succussion sounds, which simply mean that the stomach contains 
air and fluid, are elicited bimanually, with one hand supporting the 
subject's flank or back and the other sharply pushing or tapping the 
abdomen over the lower gastric area. Since identical sounds are also 
produced in the colon, it may be necessary, in the doubtful case, to 
empty either the stomach or the gut as a differential procedure. Gas- 
tric splashing is physiologic when detected within the normal bound- 
aries of the stomach and at the time this viscus should contain food. It 
is pathologic when elicited at the time the stomach should be empty, or 
when it occurs well beyond the normal gastric borders. The demon- 
stration of succussion splashing three or four hours after the patient 
has eaten suggests gastric atony or motor inadequacy; and the pres- 
ence of this sign outside the normal limits of the stomach (especially 
below the navel) is strongly indicative of the organ's enlargement 
or dislocation. 

Here may be mentioned Stiller's sign — undue mobility of the 
tenth rib — which is a frequent accompaniment of gastro-enteroptosis, 
with or without gastric atony and nervous dyspepsia. 

The Use of the Stomach -tube. — This instrument is employed 
in securing the gastric contents for analysis; in the process of thera- 
peutic lavage; in rapidly emptying and cleansing the stomach and 
introducing antidotes in poison cases; and as a substitute for the 
esophageal bougie in exploring the gullet. Under the first-named 
circumstance the gastric contents should be withdrawn by passing 
the tube upon the expiration of a definite interval after the patient 
has eaten a standard test-meal — one hour after the "roll and tea 
breakfast " ' of Ewald-Boas, or four hours after the test-meal 
of Riegel. 2 The specimen withdrawn at this time is measured, 
inspected for naked-eye changes, tested chemically, and exam- 
ined microscopically. The technic of these procedures, which is not 
germane to the plan of this work, may be found in text-books on Clin- 
ical Laboratory Methods. 

1 One dry roll (40 gm.) and a cup (400 mils) of clear tea. 

2 One dry roll (40 gm.), boiled lean meat (200 gm.), one plate of gruel soup 
(400 mils), and one glass of water (200 mils). 



54° PHYSICAL DIAGNOSIS 

The stomach-tube, made of soft rubber, measures about 3 feet 
(90 cm.) in length and J inch (8 mm.) in diameter, having at the 
lower extremity a double fenestration and at the upper a funneled 
expansion; a circle of white rubber inlaid at a point 22 inches 
(55 cm.) from the gastric end of the tube should be flush with the 
subject's incisor teeth when the instrument is introduced far enough 
to reach the stomach. Before using it is well to warm the tube by 
placing it in hot water, and to lubricate its tip by smearing it with a 
few drops of glycerin. When there is reason to anticipate obstinate 
choking or other interference with the introduction of the tube, pre- 
liminary spraying of the posterior pharynx with a 2 per cent, eucain 
solution is a useful preventive step. The patient, seated with the 
head bent forward, the mouth open, and the tongue unprotruded, is 
instructed to breathe deeply and regularly, whereupon the tube is 
quickly slipped backward along the posterior pharynx and down 
into the esophagus, at the entrance to which a muscular contraction 
usually arrests the instrument. This obstruction is but temporary, 
however, and may be overcome without much difficulty by making 
the patient swallow and take very deep breaths; when freed, the tube 
is quickly pushed down until it has entered the stomach. The patient 
now bends forward and strains as in defecation or retches as in vomit- 
ing, with the result that the stomach contents begin to trickle from 
the funnel end of the tube, which should drain into a perfectly clean 
receptacle. A sluggish flow may be overcome by "milking " the tube 
or, preferably, by aspirating into a Potain vacuum bottle. Tubes 
equipped with a bulb should not be used, for sanitary reasons. 
After the stomach has been thus emptied lavage is to be given, by 
pouring in and siphoning out sterile water, until the washings return 
clear. 

Having finished the above procedures, the tube is removed by a 
continuous sweep of the examiner's arm, the head of the patient mean- 
while being turned slightly in the opposite direction. 

The use of the stomach-tube is absolutely interdicted in angina 
pectoris, thoracic aneurism, advanced cardiovascular disease, and 
recent hemorrhage from any source, since in any of these conditions 
the stress of the operation may be perilous; it is to be used most 
cautiously, if at all, in the pregnant woman, in markedly cachectic 
and enfeebled persons, and in those suffering from active broncho- 
pulmonary lesions. A suspicion of esophageal diverticulum or of 
ulcer or cancer of the gullet or stomach calls for great care in tubing 
the patient, for fear of mechanically injuring the parts. 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 54 1 

Percussion.— To map out by percussion the tympanitic area of 
an empty normal stomach is out of the question, since in this state 
the organ recedes beneath the left dome of the diaphragm. This 
being the case, the zone of tympany directly below the liver must be 
due to the transverse colon, which rises into the space created beneath 
the anterior abdominal wall by the recession of the contracted stomach. 




Hepatic flatness 
Pulmonary margin 

Traube's semilunar 

space 
Lower gastric 

border 



Fig. 208. — Percussion area of gastric tympany. 

Nor can the lower border of the undistended stomach be accurately 
delimited by percussion, owing to its curving backward away from 
the abdominal parietes. 

In the moderately distended stomach, however, a fairly accurate 
region of pure gastric tympany can be plotted out by the trained 
examiner. The following boundaries refer to the tympanitic region 



542 PHYSICAL DIAGNOSIS 

delimited with the subject in the dorsal decubitus: upper border, 
fifth interspace in the left parasternal and midclavicular lines; lower 
border, 2 or 3 inches (5 to 7.5 cm.) above the umbilicus in the median 
line and ninth costal cartilage at the left costal margin; right border, 
2 inches (5 cm.) to the right of the median line; and left border, 
seventh interspace in the left anterior axillary line. These bound- 
aries are necessarily only approximate, owing to the wide variations 
in the size, mobility, and distensibility of the stomach in different 
individuals. 

Traube's semilunar space, normally affording pure gastric tympany, 
corresponds to that part of the anterior wall of the stomach lying 
directly beneath the costal parietes (Fig. 208) . It is bounded above 
by the left lobe of the liver and the lower border of the left lung; 
below and internally, by the left costal margin; and externally, by 
the anterior border of the spleen. The tympany of this area is 
encroached upon by flatness from above in left pleural effusion, 
massive pericardial effusion, and great enlargement of the heart, 
and the right and left lateral boundaries are similarly affected by 
enlargement of the liver and of the spleen. Extensive left basal 
pneumonia impairs, and left pneumothorax apparently extends, the 
upper (pulmonary) limit of Traube's space. 

In delimiting the upper border percussion should be continued 
from below upward until alterations in the tympany indicate the 
margins of the lung, the liver, and the spleen; the deep-seated fundus 
of the stomach may yield a muffled tympany, but only exceptionally 
is it recognizable by ordinary percussion methods. To facilitate 
mapping out the lower border, the patient, standing erect, is in- 
structed to swallow, in several tumblerful draughts, about a quart 
of water, with the result that a flat zone, corresponding to the 
lowest part of the organ, will be produced by the ingested 
fluid. This flatness increases vertically as the subject swallows 
additional fluid, it decreases after the stomach is emptied with 
the stomach-tube, and it shifts or disappears as the patient 
changes posture. This hydrostatic test is essential in distinguishing 
gastric and intestinal tympany when each viscus contains air, for 
unless their contents differ (*. e., unless one contains air and the other 
liquid or solid matter) their percussion notes are so similar as to 
defy differentiation. 

In practising auscultatory percussion of the stomach the chest-piece 
of a binaural stethoscope is placed at or near the site of the pylorus, 
and light percussion begun at several points well beyond the limits 






EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 543 

of the stomach and continued toward the viscus, which when reached 
is betrayed by a higher pitched, more intense, and purer note. A line 
connecting the points at which these changes of note occur obviously 
corresponds to the outline of the organ. The auscultatory percussion 
tone over a tumor of the anterior wall of the stomach sounds much 
less resonant and less intense than the note elicited over the healthy 
part of the organ. 

Stroke auscultation, which substitutes a gentle stroking of the 
surface with the finger tips for actual percussion, is employed for the 
same purposes as auscultatory percussion, to which it is decidedly 
inferior as a method of research. 

Increase of Gastric Tympany. — Enlargement of the area of gastric 
tympany may be symptomatic of gaseous distention, pathologic 
dilatation, or dislocation of the stomach, and in all of these conditions 
the increase is chiefly in a downward direction. A horizontal exten- 
sion of tympany, especially of the right border, means dilatation of 
the pyloric region with deficient motor power (Michaelis). Several 
extrinsic factors of increased gastric tympany are also to be recalled — 
wasting of the anterior abdominal parietes, contraction of the left 
lobe of the liver, retraction and emphysema of the left lung, left 
pneumothorax, and perigastric adhesions, causing downward and 
forward traction of the stomach. 

Decrease of Gastric Tympany. — The area of epigastric tympany 
is symmetrically contracted when actual atrophy of the stomach 
exists, as in cirrhosis ventriculi and in cancer or other stenotic lesions 
of the cardia. The restriction tympany in Traube's semilunar space 
has been alluded to in a preceding paragraph. 

Auscultation. — The deglutition murmur is the most important 
single finding afforded by this seldom-used method of examining the 
stomach. It is audible over the cardia, usually as a double sound, 
and is elicited by auscultating while the patient swallows a mouthful 
of water. Normally, the primary murmur (esophageal) is heard 
about six seconds after the act of deglutition, and the secondary 
(gastric) sound, some four or five seconds later. The absence of 
these two murmurs has been noted in stenosis of the gullet and in 
enfeeblement of the muscularis of this tube. Brenner describes a 
metallic rub audible in the region of the diaphragm in cases of per- 
foration of the stomach. 

Other sounds audible over the gastric area include succussion 
sounds (described above), gurgling arising within a dilated or dis- 
placed stomach, effervescence of fermenting gastric contents, reso- 



544 PHYSICAL DIAGNOSIS 

nant echoes of the heart sounds and of bronchopulmonary rales, 
and breath sounds transmitted and amplified by a tensely distended 
stomach. 

EXAMINATION OF THE INTESTINES 

Clinical Anatomy. — The intestinal canal consists of two principal 
divisions, small and large, the former being a highly convoluted and 
compact central mass of gut, and the latter a stretch of larger caliber 
and of less twisted contour. The greater part of the intestines is 
covered by the great omentum which hangs, curtain-like, from the 
lower gastric curvature to the lower part of the hypogastric region. 

The small intestine, some 22 to 24 feet (6.6 to 7 m.) long, occupies 
chiefly the umbilical, lumbar, and hypogastric regions, and stretches 
from the pyloric end of the stomach to the ileocecal valve, its lumen 
gradually diminishing from 2 inches (5 cm.) in diameter at the first 
point to 1 inch (2.5 cm.) at the second. The duodenum, or the 
first 10 inches (25 cm.) of the small gut, runs a C-shaped course from 
the pylorus to the jejunum, and lies almost entirely to the right of 
the median line of the belly, occupying the lower epigastrium 
and the upper umbilical region. The first (upper) part of the 
duodenum is behind the eighth right costal cartilage just to the 
left of the gall-bladder; the second (descending) part courses vertically 
from the gall-bladder along the downward projection of the right 
midclavicular line, in front of the right kidney, to the level of the third 
or fourth lumbar vertebra; the third (lower) part runs obliquely 
upward from this point to the left of the second or third lumbar 
vertebra, where it twists forward to form the duodenojejunal flexure 
whose surface marking corresponds to a point 1 inch (2.5 cm.) to 
the left of the linea alba in the transpyloric line. Clinically, it 
is important to know that the duodenum encircles the head of the 
pancreas; that it lies in close relation posteriorly with the portal 
vein, common bile-duct, right kidney, and inferior vena cava, 
and anteriorly with the liver, gall-bladder, and transverse colon; 
that it is comparatively immobile, being securely anchored to 
the posterior abdominal wall. The jejunum, which includes the 
next 8 feet (2.15 m.) of the small gut, lies chiefly in the upper 
umbilical area and in the neighboring regions to the left, while the 
ileum, forming the terminal 12 feet (3.6 m.) of the tube, lies below 
and to the right. On their course toward the pelvis the coils of the 
small intestine cover the ascending and descending colon and occupy 
the greater portion of the umbilical, lumbar, and hypogastric areas. 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 545 

The small gut is so exceedingly mobile that the above regional 
arrangement must necessarily be only approximate. 

The large intestine, which is approximately 5 feet (1.8 m.) in 
length, bounds the small gut and extends from the ileocecal valve 
to the anus, its three main divisions being the cecum, the colon, 
and the rectum. The cecum, a superficial wide cul-de-sac of the 
large gut, is in the right iliac fossa below the ileocecal valve, whose 




■ 

Fig. 209. — Surface topography of the large intestine. 

location corresponds to a point on the anterior abdominal wall 
1 inch (2.5 cm.) below the middle of a line from the anterior supe- 
rior iliac spine to the navel. The vermiform appendix springs 
from the posterolateral surface of the cecum, and may stretch 
some 3 or 4 inches (7.5 to 10 cm.) in length behind the ileum, toward 
the pelvic brim, or back of the ascending colon (Fig. 209a). The 
orifice of the appendix (at Clado's point) lies about 1 inch (2.5 cm.) 
below the ileocecal valve. (C/. p. 531.) 
35 



546 



PHYSICAL DIAGNOSIS 



Of the three parts of the colon, the first or ascending passes upward 
from the cecum to the under surface of the right costal arch, where 
below the liver it bends sharply to the left to form the hepatic flexure. 
From this point the transverse portion, more or less in the form of a 
U-shaped tube, loops across the umbilical region to the left costal 
arch beneath which it twists upward, backward, and to the 




Fig. 209a. — Radiograph of the vermiform appendix and part of the large intestine. 
(Plate by Dr. W. F. Manges.) 

left as the splenic flexure, below the spleen and behind the stomach, 
and at a higher level than that of the hepatic flexure. The descending 
portion of the colon runs down the left side of the abdomen from the 
splenic flexure to the iliac crest, where, as the sigmoid flexure (or 
iliac and pelvic colon), the gut extends through the pelvis to the 
rectum, which it joins opposite the third segment of the sacrum. 

Inspection and Palpation. — The technic and general results of 
these methods have been dealt with under Examination of the Ab- 
domen. (See pp. 512, 513.) Applied to lesions of the bowel, 
combined inspection ana palpation is the most satisfactory means 
of detecting obstruction, dislocation, and circumscribed dilatation 
of the intestines, and tumors, malignant, inflammatory, or fecal. 

X-ray examination of the large intestine gives additional in- 
formation of value, and defines with great clearness the patency 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 547 

of the ileocecal valve and the state of the colon and the lower 
portions of the large bowel. In connection with serial radiography 
following the ingestion of a bismuth meal (see p. 536), one or two 
plates are exposed after the rectal injection of a barium clyster. 
Cole recommends for this purpose 3 ounces (85 gm.) of barium 
sulphate dissolved in 50 ounces (if liters) of warm water; or about 
34 ounces (1 liter) of warm water containing 5 parts of barium 
sulphate and 12 parts of mucilage of acacia may be used. The 
enema is instilled slowly by gravity through a rectal tube, and 




Fig. 210. — Abdominal distention due to dilatation of the small intestine (Jefferson 

Hospital). 

should be retained by the patient until the plates have been 
exposed. 

Intestinal obstruction, leading to meteorism of the gut above 
the site of the stricture, causes distention of the abdomen vary- 
ing in appearance according to the part of the bow r el implicated. 
The general statement holds true, that the more remote from the 
duodenum the seat of the obstruction the greater the degree of dis- 
tention. In stenosis near the ileocecal valve (the favorite site of intus- 
susception) the brunt of the distention falls upon the small intestine 
whose coils balloon the central part of the abdomen (Fig. 210) , where, 
in the thin-bellied subject, they are visible as a series of transverse 



548 



PHYSICAL DIAGNOSIS 



parallel ridges showing exaggerated peristalsis and paroxysms of 
tetanic contraction — the so-called "organ pipe" arrangement of the 
intestinal loops. To the touch the latter feel stiff and rigid one 

moment, but gaseous, fluctuating, or 
pultaceous the next, when the spasm 
temporarily ceases, with a gurgling 
sound as the tension lessens. At 
the site of the stricture, in the right 
iliac fossa, an elongated cylindric 
tumor sometimes may be felt. In 
stenosis near the sigmoid (where 
volvulus is so prone to occur) this 
portion of the large intestine and 
the descending colon become dis- 
tended to an extraordinary degree, 
usually first bulging the left iliac 
and. hypogastric regions, but event- 
ually distending the greater part of 
the abdomen, the tympanitic gut 
often taking the form of a huge 
inflated crescent, with its convexity 
toward the right loin and its con- 
cavity encircling the navel. Disten- 
tion of other portions of the colon 
is recognized by the presence of a 
cylindric swelling corresponding to 
the superficial course of this part 
of the intestinal tract. In localizing 
the seat of a stenosis of the colon, 
percussion (q. v.) may be of assist- 
ance. Inflation of the intestines 
with air and their distention with 
water also are of value as a means 
of determining the site of an intes- 
tinal obstruction. If 6 quarts of 
water can be introduced with a foun- 
tain syringe, there is no obstruction 
in the large intestine; if less than 
4 quarts can be injected, there is probably obstruction in the 
large intestine (J. Chalmers Da Costa). 

So-called idiopathic dilatation of the colon leads to enormous dis- 
tention of the large bowel, especially near the sigmoid flexure, whence 




Fig. 2ii. — Abdominal distention 
due to dilatation of the colon (Jef- 
ferson Hospital). 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 549 

the dilatation tends to spread upward. In such instances there is 
remarkable abdominal enlargement with universal tympany extend- 
ing so high as to obscure the areas of hepatic and splenic dulness 
(Fig. 211). 

Coloptosis, or downward displacement of the colon, implicates 
chiefly the transverse portion, the abnormal outlines of which are readily 
seen after the gut has been inflated with air. Commonly a dislocated 
colon sags downward as a V-shaped tube, whose convexity lies well 
below the navel; sometimes, by traction on the splenic and hepatic 
flexures, it causes stenosis at these points, and consequently may 
lead to obstruction of the large bowel. Coloptosis rarely exists 
without gastroptosis and is often a part of the universal dislocation 
of the abdominal viscera in Glenard's disease. Ptosis of the small 
intestine doubtless can take place, though it is not evidenced by any 
distinctive physical signs. 

Cecum mobile is a condition in which the mesenteric attachment 
of the cecum and the ascending colon is defective, so that the lower 
portion of the ascending colon becomes more or less freely movable 
in the abdomen (Sailer). It is not of clinical significance unless 
the motility of the cecum results in occasional temporary or, more 
rarely, in incomplete permanent obstruction. Under these circum- 
stances the cecum becomes dilated, its wall atonic, and there is a 
condition of chronic constipation with impairment of nutrition fre- 
quently associated with attacks of pain in the right lower quad- 
rant. This pain may be a dull ache or appear in the form of 
attacks of colic. 

The local symptoms are a sense of discomfort, pressure, or pain, 
chiefly in the lower portion of the abdomen. The patient almost 
invariably suffers from chronic constipation. 

It is perhaps most frequently mistaken for chronic appendicitis 
and its existence may explain the failure to relieve symptoms no- 
ticed so frequently when the appendix has been removed and found 
practically normal. 

The physical signs are tenderness in the right lower quadrant, 
usually more diffuse than in chronic appendicitis and rarely so severe. 
Rigidity in the right lower quadrant is not often detected, and when 
it is, probably suggests the existence of a complication. The cecum 
is almost invariably palpable. It is of a curious doughy consist- 
ence, can be rolled under the ringer, and may be abnormally motile. 
In a patient with thin and relaxed abdominal walls, it can some- 
times be pushed as far as 6 cm. (2.36 inches) toward the median 
line and then back again. 



550 PHYSICAL DIAGNOSIS 

During this rolling movement gurgling or the crepitation pro- 
duced by the presence of air and fluid in a sac usually can be felt. 
If the stethoscope is placed over the cecum and succussion made, a 
splash often is elicited, and upon simple auscultation loud gurgling 
sounds frequently can be heard. 

Usually the diagnosis can be confirmed without difficulty by the 
£-ray. After a barium meal the cecum, with the aid of the fluoro- 
scope, is seen to be filled with an opaque substance, and if the 
patient be turned upon the left side its displacement is sometimes 
very striking. 

Fecal impaction, which is frequently found in the colon, forms an 
elongated and freely movable gut-shaped tumor, either of stony 
hardness or of mushy consistence, more commonly the former. Such 
a mass, should it persist after free purgation, must be differentiated 
from malignant disease of the intestine by a detailed physical exami- 
nation and by a critical analysis of the accompanying symptoms. 
During the course of enteric fever a soft sausage-shaped mass in the 
right iliac fossa may betray intestinal hemorrhage, concealed by 
reason of a paretic ileum; gurgling in this situation is in nowise dis- 
tinctive of typhoid — it simply means fluid and gas within the gut. 
Appendical thickening or abscess may account for a more or less well- 
defined tender mass near McBurney's point, provided that palpation 
is not interfered with by the board-like muscular rigidity of an as- 
sociated peritonitis. 

In chronic appendicitis Bassler's method of pinching the appendix 
at a point midway between the umbilicus and the right anterior 
superior iliac spine causes acute tenderness. It is performed by 
passing the tip of the thumb, held vertically and pointing toward 
the ensiform, into the abdominal wall at the point indicated, and 
then swinging it to the right so as to pinch the appendix against the 
iliacus muscle and thus to produce sharp pain. Exquisite tender- 
ness and pain is produced at McBurney's point in chronic appendi- 
citis by distending the colon with air by means of a rectal tube and 
pump (Bastedo's sign). 

Pericolitis sinistra, an inflammation of the lower part of the descend- 
ing colon, surrounding connective tissue, and peritoneum, is com- 
parable clinically to appendicitis, except for its situation in the lower 
left abdomen. In typical cases palpation reveals tenderness, great 
muscular rigidity, and an elongated tumor in the sigmoid region, the 
associated symptoms pointing to local peritonitis, circumscribed 
abscess, or general peritonitis. Obstinate constipation and acquired 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA SSI 

diverticula of the colon are the two most common underlying causes 
of this type of colonic inflammation. 

Malignant disease is especially prone to implicate the rectum, the 
large bowel at or near the sigmoid, hepatic, or splenic flexures, and the 
duodenum. When it invades a portion within reach of palpation a 
roughly spherical or ovoid tumor is felt, whose consistence is generally 
hard and resistant, and whose shape is unalterable by manipulation, 
differing in this particular from a fecal tumor, which sometimes can be 
pitted, dented, and otherwise molded by firmly pressing it between the 
fingers. The mobility of the tumor depends upon its situation and 
upon the firmness with which it is anchored by inflammatory adhe- 
sions. Speaking broadly, cancer of the sigmoid and of the cecum are 
fixed, while cancer of the small intestine is relatively movable. When 
obstruction exists above the growth, as eventually is the case sooner 
or later, a circumscribed dilatation of the gut occurs directly above 
the stricture; this pocket, alternately distending with feces and col- 
lapsing when its contents are expelled, is responsible for puzzling 
changes in the size and the shape of the tumor, which even may quite 
disappear for days at a time. In cancer of the rectum visual exami- 
nation with the proctoscope plus digital exploration may explain the 
reason for the unbearable sacral pain and acute tenesmus from which 
the patient suffers. 

Aside from the presence of a circumscribed tumor, most cases of 
malignant disease of the bowel are attended by symptoms of ob- 
struction and by emaciation and cachexia. In perhaps the majority 
of instances enlargement of the mesenteric glands and of the superficial 
lymphatics corroborates the other findings. 

Percussion. — Percussion of the intestines is useful chiefly in con- 
firming the findings of palpation, in conditions such as those just 
mentioned. 

Percussion over the empty colon elicits a tympanitic note of higher 
pitch, somewhat less volume, and shorter duration than is found over 
the stomach. The note over the small intestine is also tympanitic, 
and of still higher pitch, less volume, and less drum-like quality. By 
ordinary percussion these acoustic differences are not sufficiently 
marked to serve as reliable criteria in mapping out the different parts 
of the gastro-intestinal tract, but they are appreciable by ausculta- 
tory percussion or, perhaps better, by ordinary percussion after dis- 
tention of the colon with air. This is accomplished by rectal inflation 
with a Davidson syringe, after having emptied the large bowel by an 
enema. Ziemssen's method of ballooning the colon with carbonic acid 
gas is scarcely to be advised as a routine procedure. The presence 



55 2 PHYSICAL DIAGNOSIS 

of feces within the intestines, of course, modifies the above findings ; 
especially in the right iliac region and left flank is the sound likely to be 
dull, since it is in the cecum and sigmoid that fecal matter tends to 
accumulate. Impacted feces in the hepatic and splenic flexures may 
account for undue extension of the hepatic, splenic, and renal areas 
of flatness. 

In intestinal obstruction percussion of the upper lumbar regions is 
of service in localizing the seat of the stenosis. A loud, deep percus- 
sion sound (dull tympany) is found here on both sides of the spine in 
stenosis of the descending colon and sigmoid, and on the right side 
only in stenosis of the transverse colon and splenic flexure (Noth- 
nagel) . 

Auscultation. — Auscultation of the intestines is seldom employed, 
except in connection with percussion, to delimit different segments 
of the intestinal canal and to detect solid tumors thereof. Like 
the stomach, the intestines afford various splashing, gurgling, and 
hissing sounds generated by the movements of fluid and gas, and, 
according to Sahli, a somewhat distinctive sizzling or whistling noise 
is occasionally heard over an intestinal stricture through which 
gas and fluid may be forced by peristalsis, so as to give rise to audible 
and perhaps to palpable vibrations. The presence of a distinct 
splashing sound just above the point of obstruction is significant of 
ileus. 

EXAMINATION OF THE LIVER AND GALL-BLADDER 

Clinical Anatomy. — Topographically, the liver is comparable 
to a wedge driven from right to left across the upper zone of the 
abdomen directly beneath the diaphragm, quite three-fourths of the 
organ's bulk lying to the right of the median line of the trunk. In 
the adult the base of the hepatic wedge occupies the right hypo- 
chondrium, the middle portion fills the upper epigastrium, and the 
sharp convexity tapers off into the left hypochondrium and pro- 
jects some 2 or 2\ inches (5 to 6.25 cm.) beyond the left sternal 
border in the fifth intercostal space. In the young child the liver, 
being disproportionately large, extends well beyond the limits of 
the right hypochondrium, and encroaches to the left almost as far 
as the spleen. The falciform ligament and the longitudinal fissure 
together divide the liver into two principal lobes, right and left, 
whose point of divergence at the inferior parietal aspect of the organ 
anteriorly is indicated by the umbilical notch. This interlobar 
indentation is situated in the epigastric region about 1 inch 
(2.5 cm.) to the right of the median line, at the level of the ninth 
rib. Just below and external to this point lies the gall-bladder, 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 553 



whose surface marking corresponds to the angle between the ninth costal 
cartilage and the external border of the right rectus abdominis muscle. 
This pear-shaped structure, approximately 3 inches (7.5 cm.) in 
length, usually reaches to, if not beyond, the lower border of the 
liver, but its exact situation is subject to considerable variation, especi- 
ally in a horizontal direction, owing to individual peculiarities and 
to the mobility of the liver, with which it must move. The upper 
convex surface of the liver lies beneath the vault of the diaphragm, 
and is anchored to this muscle and to the anterior abdominal wall by 
the falciform ligament, a peritoneal reflection springing from the 
upper hepatic border. The lower concave surface, grooved antero- 
posterior^ by the longitudinal fissure, is in relation with the stomach, 
the hepatic flexure of the colon, 
and the right kidney. The 
anterior surface, thinning out 
into a sharp edge behind the 
right costal margin, and in- 
dented at its lower border by 
the umbilical notch, lies in 
contact with the anterior ab- 
dominal wall for a distance 
of 2 or 3 inches (5 to 7.5 
cm.) below the base of the 
ensiform cartilage. The right 
lateral and posterior surfaces 
are in relation with the abdom- 
inal wall and the diaphragm, 
which separates the liver from 
the inner costal surfaces and 
the lower pulmonary edges, 
while behind the surface bears 
the impress of three inti- 
mately related structures: aD 
esophageal groove, a vena 
caval fossa, and a right supra- 
renal impression. 

The surface topography of 
the liver is represented upon 

the anterior and posterior walls of the thorax by a wedge-shaped 
area, having its apex in the left midhypochondrium and its base 
directed toward the right; laterally, the outline of the organ is irreg- 
ularly ovoid. (Fig. 212; also Fig. 73, p. 127.) The upper border 




and gall-bladder. 



554 



PHYSICAL DIAGNOSIS 



is indicated by a line beginning at the upper part of the fifth left 1 
intercostal space, somewhat internal to the midclavicular line, and 
thence encircling the right half of the chest at the following levels: 
sixth chondrosternal articulation at the sternum, fourth interspace 
in the midclavicular line, seventh interspace in the midaxillary line, 
eighth rib or interspace in the scapular line, and eighth thoracic 
vertebra at the spine. The lower border passes obliquely downward 
and toward the right from the left extremity of the upper level, crosses 
the left costal margin at the eighth costal cartilage, cuts the median 
line about midway between the xiphisternal joint and the navel 
(in the transpyloric line), and reaches the right costal margin in 
the right Poupart (midclavicular) line; thence the lower level dips 
below the tip of the tenth costal cartilage, and passes backward to 
bridge the tenth interspace in the midaxillary line and to terminate 
alongside the spine at the level of the eleventh thoracic vertebra. The 




Fig. 213. — The hepatic fades (Jefferson Hospital). 



upper part of the external surface of the liver is covered by the 
inferior edge of the right lung as far down as the sixth rib in the mid- 
clavicular line, the eighth rib in the midaxillary line, and the tenth 
rib in the scapular line. 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 555 

Inspection. — In examining the liver, inspection is of secondary 
importance to palpation and percussion. A greatly enlarged liver 
may be shown by bulging of the lower ribs in the right hypochondrium 
and by fulness in the epigastrium below the right costal margin, but 
only exceptionally are local tumors of the organ recognizable by 
inspection. The transmitted impact of a hypertrophied heart may 
be forcible enough to jar the liver visibly, and, rarely, pulsation- of 
the liver and of enlarged superficial veins are seen in conditions of 
marked venous stasis. Here also may be noted the peculiar right- 
sided sagging of the trunk of the patient ill of hypertrophic cirrhosis. 

The hepatic fades (Fig. 213) of the subject of chronic affections 
of the liver is characterized by a muddy, sallow complexion with 
more or less anemic pallor, or perhaps by the typical saffron discolora- 
tion of jaundice. The conjunctiva? are similarly tinged, the eyes are 
watery and glistening, and beneath the skin, which is commonly 
wrinkled and dry, numerous distended venules may be visible, espe- 
cially about the nose. 

Radiographs may reveal the presence of gall-stones if the calculi 
are composed largely of calcium, but cholesterin stones, which but 
feebly absorb Rontgen rays, seldom show upon the plate. 

Palpation. — Tactile sense decides the questions of hepatic tender- 
ness, pulsation, friction, and thrills, detects extension downward of 
the lower border of the liver, and determines the consistence and the 
contour of its anterior and lower surfaces. 

Tenderness and often spontaneous pain in the hepatic region are 
common symptoms of hepatic congestion and of various inflammatory 
processes, such as, for example, perihepatitis, diffuse hepatitis, acute 
yellow atrophy, and Hanot's cirrhosis. Or the tenderness may be 
due to abscess, cancer, obstructive jaundice, or fatty degeneration. 
Hepatic pain, it is to be remembered, is not always localized, but may 
be reflected upward to the right shoulder and back (Fig. 68, p. 121). 
Gall-bladder tenderness is commonly referred to Robson's point 
(q. v. s.). In many inflammatory conditions of the liver and the 
gall-bladder Bookman's maneuver is useful in eliciting acute pain 
in the hepatic area. This consists of forcing the umbilicus down- 
ward tow T ard the pubis with the crooked index-finger, so as to stretch 
the round ligament and consequently to exert traction upon the 
liver and moderate downward and forward rotation of the organ. 

Pulsations of the liver caused by the thrust of a hypertrophied 
heart are to be distinguished from those due to congestion of the 
hepatic venous channels. In the former the "jogging" character of 
the impulse, the physical signs of right ventricular hypertrophy, and 
the absence of tricuspid leakage are the cardinal diagnostic points; 



556 



PHYSICAL DIAGNOSIS 



in the latter the expansile, resilient impulse, the murmur of tricuspid 
insufficiency, and pulsation of the jugulars form a characteristic 
trinity of signs. Dynamic throbbing of the abdominal aorta also 
is to be differentiated from hepatic pulsation. The friction-rub 
of perihepatitis and the thrill elicited by palpatory percussion 
over a hydatid cyst have been described elsewhere. (See pp. 138 
and 528.) 

With complete abdominal relaxation, enlargement and descent 
of the liver are readily determined by palpating the upper abdom- 
inal zone, with the finger-tips pointing upward toward the hepatic 
area; or the bimanual method may be more satisfactory (Fig. 
214). Except in the young child and in the wasted adult, it is not 




Fig. 214. — Bimanual palpation of the liver. 

always possible to feel the sharp lower border of the normal liver 
below the right costal arch and in the epigastrium, owing to the re- 
sistance offered by the abdominal musculature and fat. With deep 
inspiration an enlarged or a depressed liver is felt to descend 
and with expiration to ascend, this respiratory movement being a 
valuable point of distinction between hepatic enlargements and intra- 
abdominal tumors not connected with the liver, and hence fixed during 
respiration. A rigid right rectus muscle must always be considered 
as a possible counterfeit of a neoplasm of the right lobe of the liver. 
In enlargements of the liver it is important to find the umbilical notch, 
on either side of which lie the right and the left lobes (see p. ,552). 

In the presence of ascites or of meteorism it may be impossible 
to feel the lower edge of the liver, although it extends far below 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 557 

the margin of the ribs. In the former condition "dipping" (p. 513) 
should be tried or aspiration may be necessary to drain off the 
interposed fluid; in the latter the liver may sometimes be felt 
by Glenard's method — strong pressure with the fingers of the left 
hand upon the right lumbar region and palpation with the left 
thumb below the right costal margin, meanwhile exerting deep 
rotary pressure with the right hand across the upper abdomen, the 
lumbar pressure forcing the liver down and the abdominal pressure 
pushing the intestine away from the belly wall and up beneath the 
liver, so that it may be felt by the examiner's thumb (Fig. 215). 
The consistence and the contour of the liver, which vary greatly in 




Fig. 215. — Glenard's method of palpating the liver. 

different pathologic conditions, are sometimes characteristic of 
certain lesions causing hepatic enlargement. The consistence of the 
liver may be dense, yielding, or fluctuating; its surface, smooth, rough, 
or nodular; and its contour, furrowed, notched, or lobulated. 

In amyloid disease the texture of the liver feels dense and unyield- 
ing, its surface is uniformly smooth and even, and its lower border is 
blunt and rounded. Increased hardness of the liver may also result 
from cirrhosis, cancer, syphilitic hepatitis or capsulitis, and leukemic 



558 PHYSICAL DIAGNOSIS 

infiltration. A local resilient, perhaps fluctuating, area elevated 
above the surface of the organ, suggests circumscribed abscess, 
hydatid cyst, or gumma. 

The contour is regular and the surface unroughened in the amyloid, 
fatty, cyanotic, and leukemic livers; in diffuse non-purulent hepatitis 
and in generalized abscess; and in the enlargements associated with 
febrile* states, biliary obstruction, pseudoleukemic anemia, Band's 
disease, and other primary anemias. In Hanot's cirrhosis the surface 
of the liver is generally smooth or but little roughened. It is rough, 
nodular, or lobulated in atrophic and syphilitic cirrhoses, in cancer, 
and in deformity due to local constriction. In so-called corset-liver 
there may be a more or less oval projection of the right lobe extend- 
ing downward several inches below the infracostal line, or in the 
extreme instance, as far as the level of the umbilicus. A slender 
tongue-like extension of the liver below the right costal border 
(RiedePs lobe) is occasionally appreciable in cholelithiasis attended 
by great enlargement of the gall-bladder. 

A normal gall-bladder, unless distended with bile, is not palpable, 
but when enlarged it may produce a circumscribed globular bulging 
just below the right costal margin, or lower, if the distention be suffi- 
cient greatly to elongate the organ, the dimensions of which occa- 
sionally are most extraordinary. Exceptionally, the gall-bladder 
enlarges in an upward direction and is, therefore, impalpable. When 
rilled with calculi, a crunching gall-stone crepitus can sometimes be 
felt. 

Percussion. — By percussion one is able to decide, by mapping out 
the boundaries of the hepatic area, whether the size of the liver is 
normal, increased, or diminished, and whether the organ is displaced 
either upward or downward. Both ordinary and auscultatory per- 
cussion are useful in the examination of the liver, the latter method 
being especially adapted to the localization of solid tumors. 

The vertical surface measurement of the hepatic area is about 4 
inches (10 cm.) in the median and midclavicular lines, 6 inches 
(15 cm.) in the midaxillary line, and 3 inches (7.5 cm.) in the 
scapular line. These figures, which refer to the average healthy 
adult, are somewhat less in extreme old age and in the deep-chested 
subject; in the young child the surface area of the liver is relatively 
more extensive than in the adult. 

The Areas of Hepatic Dulness and Flatness. — The liver, like the 
heart, presents two different percussion zones, which may be con- 
veniently designated as hepatic dulness and as hepatic flatness 
(Fig. 216). The area of hepatic dulness, corresponding to that 
part of the upper right lobe separated from the chest wall by 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA JCQ 

the lower pulmonary margin, affords, on forcible percussion, a 
dulness tempered by the resonant quality of the intervening vesicular 
structure. The area of hepatic flatness, situated below the preceding 
and overlying that part of the organ directly in contact with the inner 
costal wall, is elicited by percussion of moderate force, and yields 
no trace of pulmonary resonance, the sound thereover being unquali- 
fiedly flat and high pitched. 

To determine the upper limit of hepatic dulness, the right side of 




Fifth 



space 



Fig. 216. — Percussion areas of hepatic dulness and flatness. 

the chest is percussed from above downward, beginning at a leve 1 
sufficiently high to demonstrate, for the sake of comparison, pure 
vesicular resonance. Carrying the percussion lines vertically down- 
ward from the second or third interspace, in the right midclavicular 
line the pulmonary resonance becomes modified and obviously im- 
paired as the fourth interspace is crossed; in the midaxillary line this 
change is noted at the seventh interspace, and in the scapular 
line, at the eighth interspace. Having thus delimited the upper 
border of the hepatic area, percussion is continued downward along 
the three lines just indicated, until the level of hepatic flatness is 
reached at the sixth, eighth, and tenth ribs in the midclavicular, 



560 PHYSICAL DIAGNOSIS 

midaxillary, and scapular lines, respectively. The dull region 
bounded by the horizontal limits thus mapped out represents the 
area of hepatic dulness. The area of hepatic flatness extends down- 
ward in the midclavicular line to the right costal margin, in the mid- 
axillary line to the tenth intercostal space, and in the scapular line 
it cannot be distinguished from the flatness of the right kidney with 
which it is continuous. In the epigastrium hepatic flatness extends 
downward in the median line for a distance of about 3 inches (7.5 cm.) 
below the xiphoid. As already pointed out, it is impracticable to de- 
limit the hepatic and cardiac flatness at their junction near the sixth 
left chondrosternal articulation. In mapping out the lower border of the 
liver anterolaterally, two fallacies must be avoided: the predominant 
tympany of the gut and stomach, and the dull overtone arising from 
the abdominal musculature. To minimize these two sources of error, 
the thin lower margin of the liver should be percussed very gently, 
so that the flat hepatic sound may not be masked by loud tympany 
on the one hand, or be blended with muscle dulness on the other. 

A normal gall-bladder lies beyond the reach of percussion, but when 
enlarged it affords flatness continuous with that of the liver, unless, 
as sometimes happens, a coil of gut has become pushed in between 
the two, so as to separate them by a transverse band of tympany. 

Enlargement of the liver is indicated by lengthening of the vertical 
lines of the hepatic area with a palpable tumor below the right costal 
margin, a general increase in the hepatic volume being met with in 
circulatory disturbances and in structural lesions of the organ, in 
biliary obstruction, in certain of the primary anemias, and in various 
diseases of the blood. Thus, the liver is unnaturally enlarged 
in active and passive congestion, acute hepatitis, Hanot's cirrhosis, 
syphilis, fatty infiltration, amyloid disease, abscess, solid tumors, and 
cysts; in obstruction of the bile-ducts and in Weil's disease; and in 
leukemia, Banti's disease, kala-azar, trypanosomiasis, malarial fever, 
enteric fever, and relapsing fever. A fictitious enlargement of the 
liver may be produced by the basal dulness of right pleural effusion 
or of extensive croupous pneumonia. Subphrenic abscess may have 
the same effect, and, should an anterior intraperitoneal abscess 
form, there may be, in addition to increase in the hepatic area verti- 
cally, a triangular bulging, fluctuating, flat area lying, base down- 
ward, between the median line, the lower border of the liver, and 
the left costal arch. 

Decrease in the size of the liver accompanies acute yellow atro- 
phy, as well as advanced Laennec's cirrhosis, in which condi- 
tions the recession of the organ from the parietes leaves a space 
filled with coils of gut whose loud tympany may entirely obliter- 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 56 1 

ate every vestige of hepatic flatness. True hepatic atrophy 
must be carefully distinguished from simulated decrease in the 
size of the liver due to certain intrathoracic and intra-abdominal 
factors: the upper zone of the hepatic surface area may be de- 
cidedly encroached upon by the downward extension of hyperreso- 
nance in emphysema of the right lung, or by the impingement of a 
pneumothoracic right pleural sac; and the lower zone may be similarly 
affected by a mass of tympanitic intestine crowded upward between the 
anterior surface of the liver and the costal parietes, or by the ascent 
of free gas within the peritoneal cavity. 

Enlargement of the gall-bladder may be symptomatic of local 
hydrops, empyema, calculi, or malignant disease, and also of biliary 
obstruction incident to simple catarrhal inflammation, intestinal 
parasites, and the pressure of enlarged glands or neoplasms, as in 
cancer of the head of the pancreas or of the pylorus. In this connec- 
tion one should recall the practical application of Courvoisiefs law, 
that enlargement of the gall-bladder plus jaundice suggests biliary 
obstruction from malignant disease rather than from cholelithiasis 
of other causes. 

Displacement of the liver is betrayed by unnatural elevation or 
depression of the horizontal hepatic levels, unattended in simple 
displacement by deviation from the normal vertical measurements 
of the hepatic area. Upward displacement is referable chiefly to 
extrahepatic factors, such as excessive subphrenic pressure, intra- 
thoracic traction and pulmonary collapse, and paralysis of the dia- 
phragm. Thus, the liver may be crowded far upward by the pressure 
of ascites, meteorism, or abdominal tumor; pulled upward by a cir- 
rhosed, atelectatic right lung; or pushed to an unusually high level 
when a paralyzed diaphragm is forced upward by the unopposed 
action of the abdominal muscles. Downward displacement, which is 
much the commoner, is generally traceable to lesions of the thorax, 
the heart, or the subphrenic space; less commonly to diseases of 
the liver itself. An emphysematous lung, a right-sided intra- 
pleural neoplasm or effusion of air or of fluid may exert sufficient 
downward pressure upon the diaphragm to depress the liver be- 
low the costal margin; and, in extreme cases, a cardiac enlarge- 
ment can have the same effect. The liver may also be depressed 
by the weight of a pus accumulation beneath the diaphragm — sub- 
phrenic abscess. II epato ptosis, or prolapse of the liver, which also 
drags down the hepatic surface area, may exist alone or in associa- 
tion with ptoses of other organs, as, for example, of the stomach 
(gastroptosis), of the intestines (enteroptosis) , of the spleen (splen- 
optosis), and of the kidneys (nephroptosis). A prolapsed liver forms 
36 



562 PHYSICAL DIAGNOSIS 

a rounded, notched mass having a smooth surface in the upper 
abdominal region, the tumor being easily removed by bimanual 
manipulation, and showing a restricted respiratory rise and fall. 
Above the tumor, in the lower right hypochondrium, the normal 
area of hepatic flatness is replaced by intestinal tympany. 

Auscultation. — As applied to examination of the liver and gall- 
bladder, auscultation is resorted to only in exceptional instances, and 
then in confirmation of signs otherwise obtained. For example, 
a soft rustling perihepatitic friction-sound provoked by respiration 
is sometimes demonstrable over the right hypochondrium when the 
peritoneal capsule of the liver is the seat of fibrinous roughening. 
Gall-bladder friction-sounds and gall-stone crepitations are auscul- 
tatory findings occasionally met with in cholelithiasis, and in gall- 
bladder distention and displacement C. M. Cooper has noted a sys- 
tolic souffle attributable to pressure upon the epigastric artery. Caval 
compression may account for a venous bruit audible over the hepatic 
area, while cirrhosis of the liver is sometimes attended by venous mur- 
murs heard most distinctly just below the ensiform, and due to dif- 
ferences in pressure within the epigastric veins and tributaries (Catti) . 

EXAMINATION OF THE PANCREAS 

Clinical Anatomy. — The pancreas is an elongated structure 
about 6 inches (15 cm.) in length, shaped somewhat like a blunt 
hook, and lying chiefly in the epigastrium, about midway between 
the umbilicus and the tip of the xiphoid. The organ stretches trans- 
versely between the duodenum on the right and the spleen on the 
left, and corresponds anatomically to the level of the first and second 
lumbar vertebrae (Fig. 217). The head of the pancreas is enclosed 
by the concavity of the duodenum, and lies opposite the second 
lumbar vertebra; the neck coincides with the junction of the median 
line of the abdomen with the transpyloric line, just above and to 
the left of which lies the body ; the tail extends into the left hypo- 
chondrium as far as the hilus of the spleen. Anteriorly the pancreas 
is covered by the stomach, transverse colon, and small intestine; 
posteriorly it is in relation with the common bile-duct, portal vein, 
inferior vena cava, aorta, left kidney, and spleen. 

Physical Examination. — The normal pancreas, being so deeply 
seated, cannot be reached through the abdominal wall, except per- 
haps in the old, emaciated subject and in one whose stomach lies 
abnormally low; in such cases the organ occasionally is palpable as 
a resistant mass horizontally crossing the epigastrium. An area of 
increased resistance, less commonly an immobile tumor, in the 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 563 

central or the right epigastric region may be felt in the event of a 
pancreatic enlargement, due, for example, to acute hemorrhage and 
inflammation, to sclerosis, or to a new growth. But only when these 
signs are accompanied by such symptoms as violent abdominal pain, 
jaundice, edema, and mydriasis after the instillation of adrenalin, 



Duodenum 




Spleen 



Pancreas 



Fig. 217. — Surface topography of the pancreas. 

and by such laboratory findings as fatty stools and glycosuria, is the 
diagnosis of a lesion of the pancreas justifiable. 



EXAMINATION OF THE SPLEEN 

Clinical Anatomy. — The spleen is a viscus of ovoid shape, situated 
in the left hypochondrium, with its long axis running obliquely down- 
ward and forward from a point 1^ inches (3.75 cm.) from the left of 
the tenth thoracic spine to the tenth rib in the midaxilla (Fig. 218). 
The diaphragmatic surface is convex, and lies directly beneath the in- 
ferior surface of the diaphragm; the gastric surface, which is concave, 



564 PHYSICAL DIAGNOSIS 

borders upon the fundus of the stomach ; the renal surface, or the 
tapered upper and posterior extremity, lies in close contact with the 
left kidney, the percussion areas of the two organs merging; and the 
intestinal surface, notched and lying anteriorly, is in relation with the 
splenic flexure of the colon. The upper one-third of the spleen, 
being covered by the lung, pleura, and diaphragm, is beyond the reach 
of physical examination, but its lower two-thirds, lying immediately 
against the chest wall, is accessible. 

Inspection. — Save in examples of extreme splenomegaly, causing 
conspicuous distention of the splenic area, visual examination of the 
spleen is of no service. 

% 

i 




Fig. 218. — Surface topography of the spleen. 

Palpation. — This, by far the most useful method of exploring 
the spleen, determines the important questions of tenderness and of 
enlargement. The patient should lie in dorsal decubitus with the 
abdomen relaxed, while the examiner, standing at the right of the 
bedside, applies the palm of his right hand to the belly wall and 
forcibly pushes upward with the finger-tips beneath the left costal 
margin, the left hand meanwhile firmly raising the patient's left 
loin, so as to elevate the spleen (Fig. 219). The spleen of normal 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 565 

size cannot be felt beneath the costal border, but if it be even mod- 
erately enlarged, its impingement against the finger-tips with each 
inspiration of the patient and its recession from them with each expi- 




Fig. 219. — Bimanual palpation of ;he spleen. 

ration is clearly appreciable; if decidedly enlarged, the organ is recog- 
nized as a much bulkier tumor, which moves diagonally upward and 




Fig. 220. — Compression-palpation of the spleen. 

downward with respiration. Grasping the patient's left flank with 
forcible compression while the thumb feels for the organ, also is an 
excellent method of detecting a splenic enlargement (Fig. 220). 



5 66 



PHYSICAL DIAGNOSIS 



Tenderness and pain in the region of the spleen are met with in 
perisplenitis, and in infarction, abscess, acute congestion, and 
other forms of enlargement of the organ. Signorelli's spleen point, 
to which cutaneous pain is referred in inflammatory lesions of the 
spleen, is situated at or near the intersection of the left fifth inter- 
space and the midclavicular line. Pulsation of the spleen has been de- 
scribed as a rare rinding in Corrigan's disease. 

Enlargement of the spleen, of rapid development and moderate 
extent, is a pertinent physical sign in various acute specific infections, 
of which the following are typical examples: malarial fever, relapsing 

fever, sepsis, typhoid fever, typhus* 
fever, acute miliary tuberculosis, 
tuberculous peritonitis, erysipelas, 
diphtheria, variola, scarlatina, pneu- 
monia, epidemic cerebrospinal fever, 
acute yellow atrophy of the liver, 
and Weil's disease. In trypano- 
somiasis and in kala-azar the organ 
enlarges progressively and some- 
times to an extraordinary dimen- 
sion. Of most of the primary 
enemias this is also true — myelogen- 
ous and lymphatic leukemia, Band's 
disease, von Jaksch's anemia, and 
pernicious anemia. Amyloid dis- 
ease, Hanot's cirrhosis, syphilis, 
rickets, acromegaly, Pick's dis- 
ease, and pancreatic cirrhosis serve 
to illustrate chronic diseases of 
which moderate splenic enlarge- 
ment is symptomatic, and to these 
may be added certain lesions induc- 
ing venous congestion, such as chronic cardiac disease, hepatic cir- 
rhosis, and tumors causing pressure. In tumors of the spleen, such 
as hydatid, cancer, or lymphadenoma, and in abscess various grades 
of enlargement, generally of irregular contour, are encountered. 

Downward displacement of the normal spleen, simulating actual 
enlargement, may be the result of lesions of the left thorax that exert 
pressure upon the upper surface of the organ, as in emphysema, 
pleural effusion, pneumothorax, and extensive neoplasm. Upward 
displacement of the organ is a change secondary to meteorism and 
ascites, and to a contracted left lung or pleura. The differentiation 







Fig. 221. — Leukemic enlargement of 
the spleen (Jefferson Hospital). 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 567 

of splenic displacement and enlargement is based partly upon the 
detection of one of the above-named factors of ptosis and partly 
upon the delimitation of the organ's upper border by percussion. 
In splenoptosis the spleen may sag downward as far as the umbilicus 
or even into the pelvis, while in the axillary region of normal splenic 
dulness the note is tympanitic. The dislocated organ, provided that 
its migration has not been complicated by inflammatory adhesions, 




Midaxillary line 
Ninth rib 
Pulmonary border 
Splenic dulness 
Eleventh rib 



Fig. 222. — The area of splenic dulness. 

is readily palpable as a freely movable mass, of smooth lieniform 
contour, of which the oval shape and notched border are the iden- 
tifying marks. 

Percussion.— The patient should either stand erect or lie partly 
upon the right side (right diagonal decubitus), with the left arm 
thrown across the thorax or above the head. Percussion over the 
anterior and inferior borders of the spleen must be very gentle, in 



568 PHYSICAL DIAGNOSIS 

order to avoid the production of a dominant tympanitic tone due to 
the proximity of the stomach and colon. Clinically, the splenic 
percussion area corresponds to an oblong patch of dulness lying 
between the middle and posterior axillary lines and beneath the tenth 
rib, tenth interspace, and eleventh rib. This superficial surface of 
the spleen, unlike the corresponding cardiac and hepatic regions, 
affords dulness rather than true flatness, owing to its anatomic 
peculiarities. In defining this area, percussion is commenced in the 
upper left axilla and carried downward along the posterior axillary 
line until the pulmonary resonance changes to dulness, at the tenth 
rib, this point being the clinical upper border of the spleen. Contin- 
uing to percuss vertically downward, this dulness is replaced by 
tympany at the lower margin of the eleventh rib, to which level the 
lower border reaches. To find the anterior border, percussion is car- 
ried along the tenth rib from Traube's area toward the horizontal 
zone of dulness just delimited, until the note of gastric tympany 
changes to dulness, in the midaxillary line. The posterior border, 
which cannot be mapped out successfully, lies about ij inches 
(3.75 cm.) to the left of the midspinal line, the upper border being 
at the level of the tenth thoracic vertebra and the lower margin 
lying next to the left kidney. 

Aside from the technical difficulties inseparable from percussion 
of the spleen, the method must needs be more or less uncertain 
owing to the many extrinsic factors that may decidedly alter 
the size of the splenic area. The latter is decreased in extent by 
left-sided emphysema or pneumothorax, as well as by gaseous 
distention of the stomach or colon; and it may be increased in size 
by a long list of extrinsic causes, of which the most important 
are fluid or solid matter within the stomach or within the splenic 
flexure of the colon, consolidation or retraction of the base of the 
left lung, effusion within or great thickening of the left pleura, left- 
sided intrathoracic neoplasm, gastric cancer, and enlargement of 
the left kidney or of the left hepatic lobe. 

In distinguishing a splenic from a renal tumor, percussion deter- 
mines in the former a lieniform mass freely movable with respiration 
and uniformly dull from well below the left costal edge to above 
the upper limit of normal splenic dulness in the left axillary region; 
in the latter there is a subcostal reniform mass of limited motility, 
vertically traversed by a zone of tympany corresponding to the course 
of the colon, beneath which a tumor of the kidney is situated (Fig. 
223). A tumor of the fundus of the stomach, which may be mis- 
taken for an enlarged spleen, is localized beneath the costal arch and 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 569 

fails to show the notched border, the sharp edge, and the distinctive 
contour of a splenic tumor. In enlarged spleen versus tumor of the 
lejt lobe oj the liver, the latter is suggested by finding a mass con- 
tinuous with hepatic dulness to the right, and one which shows neither 
the lieniform shape nor the ready mobility (on bimanual manipu- 
lation) of a splenic tumor; moreover, the respiratory displacement 
of an hepatic tumor is vertical, while that of a splenic enlargement 
is diagonal. 




Splenic tumor. Renal tumor. 

Fig. 223. — Percussion findings in splenic and in renal tumor. 

Auscultation. — A jriction-sound over the splenic area may be 
symptomatic of either perisplenitis or pleurisy, for the differentiation 
of which other physical signs relating to the spleen and pleura are to 
be considered. In conditions of splenic enlargement, especially 
when associated with ptosis of the organ, there may be a systolic 
bruit over the spleen, due to torsion stenosis of the splenic artery 
(Testi). Exceptionally, a splenic systolic murmur is also audible in 
aortic regurgitation. 



570 



PHYSICAL DIAGNOSIS 



EXAMINATION OF THE KIDNEYS 

Clinical Anatomy. — The kidneys, each of which measures 
approximately 4^ inches (11.25 cm.) long by 2% inches (6.25 cm.) 
broad, occupy the loin on either side of the spinal column, and 
lie deep beneath the thick muscles of the lumbar region (Fig. 
224). Topographically, the right kidney differs from the left in 
lying at a somewhat lower level and farther from the spine, these 
differences amounting to about $ ; inch (1.25 cm.). Anteriorly 
the kidneys lie beneath the costal borders, and extend vertically from 




Fig. 224. — Surface topography of the kidneys. 

the level of the seventh, to somewhat below that of the tenth, cos- 
tal cartilage, the inner border of the right kidney being 2 inches 
(5 cm.), and that of the left, 1^ inches (3.75 cm.) external to the 
median line. The infracostal line virtually coincides with the lower 
border of the left kidney, but lies well above this part of the right 
kidney, and the greater part of both organs is internal to Poupart's ver- 
tical lines. Posteriorly, the kidneys rest upon a dense muscular bed 
composed of the psoas, quadratus, transversalis, and diaphragm; 
they extend vertically from the eleventh thoracic to the third 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 57 1 

lumbar vertebral spine, the lower borders being i£ to 2 inches 
(3-75-5 cm.) above the iliac crest, and the external borders lying 
4 inches (10 cm.) from the midspinal line. The right kidney is in 
relation with the liver, the hepatic flexure of the colon, and the duod- 
enum, and the left is adjacent to the fundus of the stomach, pancreas, 
spleen, jejunum, and splenic flexure of the descending colon. 

Inspection. — A large renal tumor causes visible bulging of one 
of the lateral regions of the abdomen, the deformity being especi- 




Fig. 224a. — Radiograph of a renal calculus. (Plate by Dr. W. F. Manges.) 



ally marked when the patient stands with the body bent forward 
so as to relax the belly wall and to favor descent of the mass. 
A tumor first appearing in the lower hypochondrium suggests primary 
implication of the upper part of the kidney, but a swelling first noticed 
in the lumbar or iliac area points to an initial invasion of the lower 
renal surface; in either case the enlargement may ultimately become 
enormous and distend any part, if not the whole, of the abdomen. 
Save in abscess, which frequently causes a posterior swelling in the 
loin, renal tumors tend to enlarge anteriorly, owing to the firm resist- 



572 PHYSICAL DIAGNOSIS 

ance offered by the muscular and osseous structures of the 
back. Secondary pressure-changes associated with renal growths 
include compression of the right lung and upward displacement of 
the liver by right-sided tumors, and the encroachment of left-sided 
neoplasms upon the heart, the left lung, the spleen, and the stomach, 

As factors of renal enlargement hydronephrosis, pyonephrosis, 
perinephric abscess, and cystic degeneration play conspicuous, and 
sarcoma and echinococcus disease less prominent, roles. 

Palpation. — The patient may lie in the dorsal position or stand 
with the trunk inclined forward, and should breathe as deeply as 
possible, so as to favor vertical displacement of the kidneys by the 
action of the diaphragm. Either bimanual palpation, with one 
hand supporting the loin and the other exploring below the costal 
arch, or the method employed in examining the spleen (gripping the 
flank with one hand) is satisfactory in palpating the kidneys. 

The renal reflex (lumbar muscle spasm) is a sign of kidney in- 
flammation, due to acute nephritis, calculus, tuberculosis, and 
similar processes. To elicit it the patient sits erect, with the lum- 
bar muscles relaxed, and the examiner palpates the lumbar region 
with a view to determining increased muscular firmness and den- 
sity on the affected side (Pottenger). 

A normal kidney is sometimes palpable in the emaciated subject 
and in one whose abdominal parietes offer little or no resistance. 
A renal tumor rises and falls with respiration to a limited degree; it 
is generally of roughly spherical shape, unless the growth happens to 
enlarge the organ symmetrically, in which event a reniform outline 
may be retained; and its consistence varies with the nature of the 
exciting lesion — it is firm and resistant in sarcoma, boggy in hydro- 
nephrosis and in cystic degeneration, and fluctuating in abscess and 
in hydatid disease. 

Aside from renal enlargements, the condition of nephroptosis is 
the chief abnormality of the kidneys discoverable by tactile sense. 
Nephroptosis, or renal prolapse, exists when the mobility of one or 
of both kidneys exceeds the normal range, which is approximately 
| inch (1.25 cm.). Although there are precise technical differ- 
ences between a movable and .a floating kidney (the latter having 
a mesonephron and the former none), the clinical criteria afforded 
by physical examination relate to the range of renal mobility and 
accessibility. Thus, three clinical types of renal ptosis are recog- 
nized: palpable kidney, palpable but not movable below the costal 
margin; movable kidney, whose entire anterior surface is easily 
palpable and which can be displaced toward or to the level of the 



EXAMINATION OF ABDOMEN AND ABDOMINAL VISCERA 573 

navel; and floating kidney, which can be readily pushed over to or 
beyond the median line and also depressed well below the umbilical 
level. Prolapse of the kidney, which is more often right- than left- 
sided, is recognized by palpating an abdominal reniform mass which 
may be replaced to the normal site of the kidney and readily pushed 
from place to place with the hand. Such a tumor may or may not 
be larger than the healthy kidney, is usually sensitive when squeezed, 
and occasionally shows the outline of the hilus and perhaps the throb 
of the renal artery; it is especially well defined when the patient ceases 
to breathe at the end of a forced inspiration, and may tilt forward 
when the subject takes the knee-chest position and drop backward 
when dorsal decubitus is assumed. As corroborative signs of renal 
displacement the so-called "lumbar recess" and a tympanitic percus- 
sion note over the renal area in the back are of importance. 

An enlarged kidney must be distinguished from tumors of the 
liver and of the spleen; a displaced kidney, from an enlarged gall- 
bladder and from tumors of the ovary, the stomach, and the intestines. 
A tumor of the liver lengthens the vertical extent of the hepatic area, 
tends to invade the thorax above and to bulge it below, and to pro- 
duce a subcostal mass corresponding to the contour of the liver and 
moving freely with respiration. A tumor of the spleen is recognized 
by its characteristic shape, oblique position, free respiratory excur- 
sion, uniform dulness on percussion, and encroachment upon the 
left thorax (v. s.). A distended gall-bladder, though to some 
extent displaceable, does not remain so, but returns of itself to 
the edge of the liver when the restraining pressure is removed 
after it has been pushed downward; nor can the gall-bladder be pushed 
upward out of reach. The respiratory mobility of the mass is con- 
siderable and its dulness is generally continuous with that of the liver. 
In the case of an ovarian tumor the mobility of the mass is restricted, 
usually to a level not much higher than that of the pelvis; the relation 
of the tumor to the uterus can be established by vaginal palpation; 
and its close proximity to the anterior abdominal wall can be proved 
by mapping out by percussion an area of dulness surrounded by a 
zone of intestinal tympany. Gastric and intestinal tumors lack the 
characteristic mobility of a floating kidney, they do not alter renal 
dulness in the loin, and they can be traced to their source by inflation 
of the stomach or of the gut, as circumstances indicate. 

Percussion. — In attempting percussion of the kidneys the diagonal 
decubitus is perhaps the most satisfactory posture for the patient 
to assume, in order to relax the tense lumbar muscles; but even in 
this position it is impossible to reach the normal kidneys by percus- 



574 



PHYSICAL DIAGNOSIS 



sion, owing to their deep situation. The chief value of percussion 
of the kidneys relates to determining the presence or absence of 
colon tympany over a mass below the left costal arch, which may 
be a tumor either of the left kidney or of the spleen. (See Fig. 223.) 
A kidney large enough to extend, or so greatly displaced as to diminish, 
the renal area, can be detected by palpation. Posteriorly, renal dulness 
is inseparable from that of the overlying lumbar muscles, the interven- 
ing spinal column, and the adjacent spleen and liver (Fig. 225). A 



Spleen 



Descending colon 




Eleventh thoracic 
vertebra 
welfth rib 

hird lumbar vertebra 
Ascending colon 



Fig. 225. — The renal area posteriorly, showing rectangle of percussion dulness 
between the eleventh thoracic and third lumbar vertebrae. 



dull zone, extending vertically from the eleventh thoracic to the third 
lumbar spine and horizontally for a distance of about 3 inches 
(7.5 cm.) on either side of the spine, overlies the kidneys, whose outer 
and lower borders occasionally can be delimited from colon tympany 
by percussing from the level of the twelfth rib outward toward the 
flanks and downward toward the iliac crests. Dulness in the 
scapular line below a point ij inches (3.75 cm.) above the iliac 
crest may mean an enlarged kidney — or a colon packed with 
feces. Loss of dulness in the renal area has been found in nephrop- 
tosis. 



INDEX 



Abdomen, areas of, 510 
ascitic, 518 
auscultation of, 515 
clinical anatomy, 507 

types, 515 
cutaneous flexion-folds of, 509 
dipping of, 513 
edema of, 525 

enlarged and tortuous veins over, 526 
enlargements of, 521 

above pubes, 523 

below left costal arch, 523 
right costal arch, 522 

from cancer of intestines, 524 
of peritoneum, 524 

from distended bladder, 524 

from gravid uterus, 524 

from leukemic spleen, 524 

from ovarian cyst, 524 

from tumors, 523 

in flank, 523 

in umbilical region, 523 
enteroptotic, 520 
examination of, 507 

in dorsal position, 512 

in erect position, 512 

in knee-chest position, 512 

in lateral position, 512 

methods, 512 
fat necrosis of, 526 
fluctuation of, 527 
gaseous, 519 
gastroptotic, 520 
inspection of, 512 
mensuration of, 514 
movements of, 524 
muscular rigidity of, 527 
obese, 516 
of pregnancy, 517 
pain in, 528 
palpation of, 513 

bimanual, 514 
percussion of, 514 
puncture of, 56 
scaphoid, 516 



Abdomen, skin of, 525. See also Skin 
of abdomen. 
subcutaneous nodules of, 526 

tissue of, 525 
tactile friction of, 528 
topographic lines and areas, 510 
Abdominal aorta, aneurism of, 505 
diagnosis, 505 
physical signs, 505 
pulse in, 505 
clinical anatomy, 509 
fluid, examination of, 59 
friction, 515 
respiration, 95, 97 
thrills, 528 
viscera, examination of, 507 

topographic lines and areas, 510 
Abscess, myocardial, 429 
of lung, 262 

after croupous pneumonia, 209 
clinical pathology, 262 
diagnosis, 264 
physical signs, 263 
pericardial, 413 
subphrenic, 301 
Absence of septa between auricles and 

ventricles, 486 
Absent respiration, 162 
Acromion auscultation, 28 
Actinomycosis, pulmonary, 271 

physical signs, 271 
Adenitis, 505 

tracheobronchial, 306 
Adherent pericardium, 414 
Adhesive pericarditis, chronic, 414 
Broadbent's sign in, 416 
clinical pathology, 414 
diagnosis, 417 
Friedreich's sign in, 416 
Kussmaul's sign in, 416 
physical signs, 415 
Sander's sign in, 416 
pleurisy, chronic, 290 

clinical pathology, 290 
diagnosis, 292 

575 



576 



INDEX 



Adhesive pleurisy, chronic, physical 

signs, 291 
Adventitious sounds, 164 
Air-hunger, Kussmaul's, 104 
Air-passages, upper, stenosis of, as 

cause of dyspnea, 104 
Alar scapulae, 80 

thorax, 80 
Albinism, pulmonary, 244 
Alimentary canal, test-meals for #-ray 

examination of, 536 
Allorhythmia, 372 
Allorhythmic pulse, 346 
Alternating pulse, 378 
Alternation arhythmia, 378 

of the heart, 346 
Amphoric resonance, 150 

respiration, 158 
Amphoriloquy, 164 
Anacrotism in aortic stenosis, 472 
Anemic dyspnea, 103 

murmur, diastolic, 393 
Aneurism, arteriovenous, 490 
of abdominal aorta, 505 
diagnosis, 505 
physical signs, 505 
pulse in, 505 
of aorta, 488 

of common carotid artery, 502 
of innominate artery, 502 
of physical signs, 501 
of pulmonary artery, 502 
of subclavian artery, 502 
of superior vena cava, 502 
of symptoms, 501 
of thoracic aorta, 488 
ascending arch, 492 
buccal souffle in, 500 
clinical pathology, 488 
descending, 492, 493 

arch, 492, 493 
diagnosis, 501 
dissecting, 490 
Drummond's sign in, 500 
false, 490 
fusiform, 489 
Glasgow's sign in, 500 
Oliver's sign in, 498 
physical signs, 493 
pulse in, 498 
saccular, 489 
Sansom's sign in, 500 
tracheal elevation in, 498 

tugging in, 498 
transverse arch, 492, 493 
true, 490 
Rasmussen's, in chronic ulcerative 
tuberculosis, 228 



Aneurism, varicose, 491 . 
Aneurismal phthisis, 504 

varix, 490 
Angle, cardiohepatic, 360 
dulness of, 147 
epigastric, 75 
Louis', 73 

pulsations in, 331 
subcostal, 75 

- respiratory alterations of, 96 
Angulus Ludovici, 73 
Anthracosis, 259 

Aorta, abdominal, aneurism of, 505 
diagnosis, 505 
physical signs, 505 
pulse in, 505 
clinical anatomy, 509 
aneurism of, 488 
ascending, clinical anatomy, 319 
dilatation of, 472 
double, 490 
thoracic, aneurism of, 488. See 

also Aneurism of thoracic aorta. 
transposition of, 487 
Aortic arch, dynamic dilatation of, 463 
area, 364 

incompetence, relative, 463 
murmurs, 387, 392 
diastolic, 392 
systolic, 392 
regurgitation, 461 

capillary pulse in, 465 
clinical pathology, 461 
Corrigan's pulse in, 466 
diagnosis, 469 

difference in arm and leg blood- 
pressure in, 467 
Doroziez's sign in, 469 
locomotive pulse in, 464 
Misset's sign in, 464 
movable pulse in, 464 
physical signs, 464 
pulse in, 466 
see-saw murmur in, 468 
systolic blood-pressure in, 467 
Traube's sign in, 469 
venous pulse in, 465 
roughening, 392 

sound, second, enfeeblement of, 369 
stenosis, 469 

anacrotism in, 472 
clinical pathology, 469 
diagnosis, 473 
physical signs, 472 
pulse in, 472 
pulsus bisferiens in, 472 

tardus in, 472 
relative, 472 



INDEX 



577 



Aortic valve, clinical anatomy, 318 
Apex pneumohia, 204 
Apex-beat, 325 
absent, 327 
cardiogram of, 328 
character of, 327 
diastolic rise of, 328 
displacement of, 326 
downward, 326 
left lateral, 326 
right lateral, 326 
upward, 326 
downstroke of, 328 
enfeebled, 327 
exaggeration of, 327 
upstrole of, 328 
Apical expansion, Bethea's method of 
determining, 133 
systolic murmur, 386 
Apneumatosis, 255, 256 
Apoplexy of lung, 192 

pulmonary, 195 
Appendicitis, chronic, Bassler's sign 
in, 55o 
Bastedo's sign in, 550 
Appendix, vermiform, clinical anat- 
omy, 545 
Arachnoid pulse, 352 
Arhythmia, 371 
alternation, 378 
cardiac, blood-pressure in, 34 
extrasystolic, 372 
fibrillation, 377 
heart-block, 375 
complete, 376 
incomplete, 376 
hemisystolic, 379 
intermittent, 372, 374 
respiratory, 99, 372 
sinus, 372 

in effort syndrome, 407 
youthful type, 372 
Arm, upper, enlargement of veins, 107 
Arnold's phonophore, 26 
Arterial blood-pressure, instrumental 
estimation, 31 
murmurs, 400 
diastolic, 401 
systolic, 400 
pulse, 336 
sphygmogram, 40 
tension, 322, 337 
wall, caliber of, changes in, 339 
changes in, 339 
Arteriosclerosis, 339 
Arteriovenous aneurism, 490 
Artery, carotid, common, aneurism 
of, 502 

37 



Artery, epigastric, deep, clinical an- 
atomy, 509 

iliac, common, 509 

innominate, aneurism of, 502 
clinical anatomy, 319 

pulmonary, aneurism of, 502 
clinical anatomy, 319 
transposition of, 487 

subclavian, aneurism of, 502 
Arthritis in croupous pneumonia, 209 
Aschner's oculocardiac reflex, 345 
Aschoff's nodules, 431 
Ascitic abdomen, 518 
Asphyxial stage of gassing, 193 
Asphyxiation, gas, bradycardia in, 345 
Aspiration pneumonia, 200 
Aspirator, Potain's, 49 
Asthenia, neurocirculatory, 406 
Asthma, bronchial, 181. See also 
Bronchial asthma. 

cardiac, 106 

catarrhal, 181 

essential, 181 

grinder's, 259 

idiopathic, 181 

renal, 104 

spasmodic, 181 
Asthmatoid wheeze, 102 
Atelectasis, 255 

acquired, 255 

compression, 256 

congenital, 256 

diagnosis, 259 

lobar, 259 

obstruction, 256 

obturation, 187 

physical signs, 258 
Atelectatic crepitation, 168 

subcrepitations, 169 
Athlete's heart, 462 
Atrophic emphysema of lungs, 247, 253 

thorax of, 82 
Atrophy of heart, 487 

progressive muscular, thorax of, 88 

senile, of lungs, 253 
Atropin reaction in cardiac com- 
petency, 341 
Auenbrugger's sign, 411 
Auricles of heart, clinical anatomy, 317 
Auricular diastole, 322 

extrasystole, 374 

fibrillation, 377 

flutter, 342 

systole, 321 

tachycardia, 342 
Auriculoventricular buncle of His, 321 

extrasystole, 374 

groove, clinical anatomy, 318 



578 



INDEX 



Auriculo ventricular node, 321 
Auscultation, 22 

acromion, 28 

immediate, 23, 28 

mediate, 23, 27 

of abdomen, 515 

of cardiovascular system, 363 

of heart, 363 

of liver, 562 

of lungs, 155 

of spleen, 569 

of stomach, 543 

rod, 16 

stroke, 16 

of stomach, 543 

technic, 27 

transmanual, 28 

tuning-fork, 28 
Auscultatory areas, 364 

percussion, 15 
of stomach, 542 

sphygmomanometry, 33 
Autophonometry, 29 
Aviators, hypertension in. 36 

in effort syndrome, 461 
Axilla, dulness in, 147 
Axillary glands, enlargement, 115 

line, anterior, 76 
posterior, 76 

region, 79 
Axis, celiac, 509 



Baas' theory of vesicular breathing, 

Baccelli's sign, 164 

in serofibrinous pleurisy, 282 
Back, percussion of, 138 
Band-box resonance in hypertrophic 

emphysema of lungs, 251 
Barnard-Hill sphygmometer, 35 
Barrel-chest, 80, 81 
Bassler's sign, 550 
Bastedo's sign, 550 
Bathycardia, 325 

Beaded excrescences of valves, 435 
Bell tympany, 154 
Bethea's method of determining apical 

expansion, 133 
Biermer's sign, 154 
Bigeminal pulse, 346 
Biot's respiration, 101 
Black phthisis, 259 
Blocked pleurisy, 51 
Blood-pressure, 322 

arm-leg, in aortic regurgitation, 467 

arterial, instrumental estimation, 31 

in cardiac arhythmias, 34 



Blood-pressure, Kilgore's fractional 
method, 34 

venous, instrumental estimation, 37 
Oliver's method of estimating, 37 
Boat-shaped thorax, 88 
Body, position of, influence on cardiac 

physical signs, 324 
Bookman's maneuver in eliciting pain 

in hepatic area, 555 
Bowles' stethoscope, 24 
Bradycardia, 344 

in gas asphyxiation, 345 

Stokes-Adams', 376 
Breast, chicken-, 84 

funnel-, 85 

keel, 84 

pain in, 120, 121 

pigeon-, 84 
Breathing, 94. See also Respiration. 
Brenner's metallic rub in perforation of 

stomach, 543 
Broadbent's sign, 332, 416 
Bronchi, clinical anatomy, 128 

stenosis of, 187 
Bronchial asthma, 181 

clinical pathology, 181 
Curschmann's spirals in, 182 
diagnosis, 183 
Laennec's perles in, 182 
physical signs, 181 

catarrh, acute, 175 
chronic, 178 

dilatation, 183 

glands, tuberculosis of, 306 

rales, 166 

respiration, 157 
Bronchiarctia, 187 
Bronchiectasis, 183 

clinical pathology, 183 

cylindric, 183 

diagnosis, 186 

fusiform, 183 

globular, 183 

physical signs, 185 

saccular, 183 

universalis, 183 
Bronchiectatic cavities, tympany in, 

149 
Bronchiloquy, 164 
Bronchiolectasis, 183 
Bronchitis, catarrhal, acute, 175. See 
also Catarrhal bronchitis, acute. 
chronic, 178. See also Catarrhal 
bronchitis, chronic. 
fetid, 179 

Dittrich's plugs in, 179 
fibrinous, 179. See also Fibrinous 
bronchitis. 



INDEX 



579 



Bronchitis, gas, 193, 194 
plastic, 179 
putrid, 179 

Bronchocavernous respiration, 158 

Bronchophony, 163 

Bronchopneumonia, 197 
confluent, 202 

Bronchopneumonic phthisis, acute, 
223. See also Phthisis, acute bron- 
chopneumonic. 

Bronchopulmonary system, diseases, 

175 
examination, 124 
Bronchorrhea, 179 
Bronchostenosis, 187 

clinical pathology, 187 

diagnosis, 188 

physical signs, 188 
Broncho vesicular respiration, 156, 159 
Brown induration of lungs, 190 
Bruit. See also Murmur. 

buccal, in aneurism of thoracic aorta, 

.5°° . 
Bruit d'airain, 154, 299 

de cuir neuf, 409 

de diable, 402 

de drapeau, 167 

in fibrinous bronchitis, 180 

de galop, 370 

de moulin, 400 

in pneumopericardium, 419 

de pot fele, 151 

de rappel, 370 

de tabourka, 503 

systolic, over gall-bladder, 562 
over spleen, 569 

venous, over hepatic area, 562 

viole, 159 
Bryson's sign, 98 
Buccal rales, 166 

souffle in aneurism of thoracic 
aorta, 500 
Bulging, unilateral, of thorax, 88 
Buth's method of paracentesis abdomi- 
nis, 58 
Button-hole mitral defect in mitral 

regurgitation, 451 



Calcium content of cerebrospinal fluid, 

64 
Calmette's ophthalmoreaction, 70 
Cambridge electrocardiographic outfit, 

44 
Canter rhythm, 370 
Capillary pulse, 353 

in aortic regurgitation, 465 
Caprizant pulse, 351 



Caput medusae, 526 
Carcinoma cells in pleural fluid, 54 
of lungs, 267 

physical signs, 269 
of pleura, 302 
of stomach, pain in, 538 
.y-ray examination in, 537 
Cardia, clinical anatomy, 531 
Cardiac. See Heart. 
Cardiogram, 41 

of apex-beat, 328 
Cardiography, 37 
Cardiohepatic angle, 360 

dulness of, 147 
Cardiopneumatic rales, 170 
Cardiorespiratory murmurs, 399 
Cardiosplanchnic paresis, 406 
Cardiovascular system, auscultation 
of, 363 
auscultatory areas of, 364 
clinical anatomy, 316 
diseases of, 405 
examination of, 316 
inspection of, 323 
palpation of, 323 
percussion of, 358 

methods and technic, 360 
valve areas of, 364 
Carditis, 429, 435 
Carnification, pulmonary, 257 
Carotid artery, common, aneurism 
of, 502 
pulsations, 330 
wave, 43 
Catarrh, bronchial, acute, 175 
chronic, 178 
dry, 179 
mucous, 179 
suffocative, 197, 200 
Catarrhal asthma, 181 
bronchitis, acute, 175 

clinical pathology, 175 
diagnosis, 177 
physical signs, 176 
chronic, 178 
clinical pathology, 1 78 
diagnosis, 179 

in croupous pneumonia, 209 
physical signs, 178 
pneumonia, 197 

clinical pathology, 197 
diagnosis, 202 
physical signs, 201 
Catarrhe pituiteux, 179 

sec, 179 
Cavern iloquy, 164 
Cecum, clinical anatomy, 545 
mobile, 549 



5 8o 



INDEX 



Cecum mobile, physical signs, 549 

Celiac axis, 509 

Cells, cancer, in pleural fluid, 54 

heart disease, 191 
Cerebrospinal fluid, 63 

bacteriologic examination, 65 

calcium content of, 64 

chemic composition, 64 

cytodiagnosis of, 64 

potassium content of, 64 

volume, 64 

Wassermann reaction in, 65 
Cervical glands, enlargement, in 
rib, pressure of, on subclavian artery, 

504 

veins, respiratory turgescence, 131 
Chalicosis, 259 
Chest, examination of, 72. See also 

Thorax. 
Cheyne-Stokes' respiration, 99 
Chicken-breast, 84 
Chyliform pleurisy, 276 
Chylopericardium, 417 
Chylothorax, 294 

Cicatrices fistuleuses in fibroid phthisis, 
241 

of thorax, 123 
Circulation, greater, 322 

lesser, 322 

mechanism of, 319 

pulmonary, 322 

systemic, 322 
Cirrhosis of lung, 219 

after croupous pneumonia, 209 
Clado's point, 53 1 

Clavicles as landmarks of thorax, 73 
Clavicular line, 76 
Click, mucous, 168 
Cloud gases, effects of, 193, 200 
Clubbed fingers, 123 
Coal-miners' lung, 259 
Coccygeal region, pain in, 123 
Cog-wheel respiration, 162 
Collapse, diastolic, of jugular veins, 

33i 

pulmonary, 255 
Collapsing pulse in aortic regurgitation, 

466 
Colon, clinical anatomy, 546 

idiopathic dilatation, 548 

percussion of, 551 
Coloptosis, 549 
Color changes in skin of abdomen, 

526 
Compensation of heart, 442 

ruptured, 442 
Complementary pleural space, 129 
Complete heart-block, 375 



Compression atelectasis, 256 
Confluent bronchopneumonia, 202 
Congestion, pulmonary, 189. See also 

Lungs, congestion of. 
Contraction, unilateral, of thorax, 90 
Contusion pneumonia, 216 
Copenhagen heart, 450 
Cor bovinum, 420 
hirsutum, 408 
villosum, 408 
Core pneumonia, 205 
Corrigan's button-hole mitral defect 
in mitral stenosis, 451 
pulse in aortic regurgitation, 466 
Corset-liver, 558 
Costal arch, 508 

enlargement of veins of, 108 
line of, 78 
pain in, 121 
line, third, 76 

sixth, 78 
respiration, 95, 97 
Cough phenomenon, 233 

winter, 178 
Courvoisier's law, 561 
Cracked-pot resonance, 151 
Crepitant rales, 167 
Crepitations, gall-bladder, 562 
subpleural, 172 
xiphoid, 528 
Crepitus, 166. See also Rales. 
Cricoclavicular line, 76 
Crossed pneumonia, 204 
Croupous pneumonia, 203 
abscess of lung after, 209 
arthritis in, 209 
cardiac sounds in, 213 
catarrhal bronchitis in, 209 
cirrhosis of lung after, 209 
clinical pathology ,_ 203 
consonating rales in, 213 
crepitus redux in, 212 
diagnosis, 213 
endocarditis in, 209 
fibrinous pleurisy in, 209 
gangrene of lung after, 209 
myocarditis in, 209 
pericarditis in, 209 
phthisis after, 209 
physical signs, 210 
pulse in, 211 
sputum in, 210 _ 
stage of congestion, 205 
of delayed resolution, 208 
of gray hepatization, 208 
of purulent infiltration, 208 
of red hepatization, 206 
#-ray examination in, 211 



INDEX 



58l 



Curschmann's spirals in bronchial 

asthma, 1S2 
Cyanosis, 106 
Cycle, cardiac, 319 

respiratory, 94 
Cyrtometry, 30 

Cysts, echinococcus, examination of 
fluid from, 60 
of lung, 272 
hydronephrotic, examination of fluid 

from, 60 
of pancreas, examination of fluid 

from, 60 
ovarian, examination of fluid from, 

59 
Cytodiagnosis, 50 

of cerebrospinal fluid, 65 
of pleural fluid, 53 



Death-rattle, 169 
Debility, cardiac, 406 
Decompensation of heart, 442 
Decubitus, influence of, on vocal frem- 
itus, 135 
Decurtate pulse, 352 
Degeneration, myocardial, granular, 

429 
Deglutition murmur of stomach, 543 

pneumonia, 200 
Delirium cordis, 372 
d'Espine's sign, 308 
Dextrocardia, 486 
Diabetic dyspnea, 104 
Diaphragm phenomenon, 95 
Diaphragmatic pleurisy, 288 

respiration, 95 
Diastole, auricular, 322 
prolongation of, 379 
ventricular, 322 
Diastolic anemic murmur, 393 
collapse of jugular veins, 331 
murmurs, 383 
aortic, 392 
arterial, 401 
pulmonic, 396 
rise of apex-beat, 328 
Dichlorethylsulphid, effects of, 200 
Dilatation, bronchial, 183 
cardiac, 425 
auricular, 428 
clinical pathology, 425 
diagnosis, 428 
physical signs, 427 
ventricular, left, 427 

right, 428 
with hypertrophy, 426 
with thinning, 426 



Dilatation, dynamic, of aortic arch. 463 
idiopathic, of colon, 548 
of aorta, 472 
of lungs, acute, 254 
Dipping of abdomen, 513 
Disordered action of heart, 406 
Dissecting aneurism of thoracic aorta, 

490 
Dittrich's plugs in fetid bronchitis, 

179 
Double aorta, 490 

murmur, Duroziez's, 401 
pneumonia, 204 
shock sound, Sansom's, 456 
Drift gases, effects of, 193, 200 
Dropsy of lungs, 192 
pericardial, 417 
pleural, 292 
Drummond's sign in aneurism of 

thoracic aorta, 500 
Drumstick ringers, 123 
Dry catarrh, 1 79 

rales, 166 
Ductus arteriosus, patency of, 485,487 
Dudgeon's sphygmograph, 40 
Dulness, 13, 19 

cardiac, area of, 359 
decrease in, 362 
increase in, 361 
from impairment in interscapular 

area, 147 
hepatic, 558, 559 
in axilla, 147 

of cardiohepatic angle, 147 
of lung, 144 
apical, 146 
at base, 147 
parasternal, 147 
paravertebral, 147 
sternal, 147 
unilateral, 147 
of normal tympany in Traube's 

space, 147 
parasternal, 147 
paravertebral, 147 
pulmonary, 144. See also Dulness 

of lung. 
relative, 19 
sternal, 147 
thymus, 504 
vascular, area of, 360 
Duodenojejunal flexure, clinical anat- 
omy, 544 
Duodenum, clinical anatomy, 544 
Duroziez's double murmur, 401 
sign, 402 

in aortic regurgitation, 469 
Dyspnea, 102 



582 



INDEX 



Dyspnea, anemic, 103 
cardiac, 105 
constant, 102 
diabetic, 104 
expiratory, 102 
functional, 103 
in fevers, 103 
inspiratory, 102 
mechanical, 104 
mixed, 102 
objective, 102 
obstructive, 104 
paroxysmal, 102 
pulmonary, 105 
stenotic, 104 
subjective, 102 
toxemic, 103 
types, 102 
uremic, 103 



Echinococcus cysts, examination of 
fluid from, 60 

of lung, 272 
Eclat clangoreaux diastolique, 409 
Ectasia, alveolar, of lungs, 248 
Ectopia cordis, 486 
Edema of abdomen, 525 
of lungs, 192 

acute fulminating, 193 

clinical pathology, 192 

collateral, 193 

congestive, 193 

diagnosis, 195 

focal, 193 

gas, 193 

Huchard's paradoxic percussion 
sound in, 194 

inflammatory, 193 

physical signs, 193 

pulse in, 193 

suffocative, 193 
of thorax, 108 

general, in 

local, 108 
Effervescence of gastric contents, 543 
Effort syndrome, 403, 406, 461 

sinus arhythmia in, 407 
Effusion, pericardial, serous, 410 
Egophony, 164 
Electrocardiogram, 45 
Electrocardiograph outfit, 44 
Electrocardiography, 44 
Ellis' line in serofibrinous pleurisy, 

280 
Embolic pneumonia, 195 
Embryocardia, 379, 428 
Emphysema, atrophic, thorax of, 82 



Emphysema, compensatory, hyperres- 
onance in, 148 
glass-blowers', 249 
large-lunged, 248 
pulmonary, 248 
acute, 247, 254 
atrophic, 247, 253 
collateral, 253 
compensatory, 247, 253 
complementary, 253 
hypertrophic, 247, 248 

band-box resonance in, 148, 251 
clinical pathology, 248 
diagnosis, 252 
hyperresonance in, 148 
idiopathic, 248 
interlobular, 255 
interstitial, 247, 255 
intervesicular, 255 
local, 253 

physical signs, 250 
pseudohypertrophic, 248 
substantive, 248 
true, 248 

vesiculo tympany in, 251 
vicarious, 253 
small-lunged, 247, 253 
Emphysematous crackling, 167 

thorax, 80, 82 
Empyema necessitatis, 122, 286 
of pericardium, 413 
of thorax, 285 

clinical pathology, 285 
physical signs, 287 
pulsating, 286 
Endocardial murmurs, 380 
Endocarditis, acute, 433 
diagnosis, 438 
mural, 433 
physical signs, 436 
chronic, 439 

clinical pathology, 439 
interstitial, 439 
primary effects, 442 
secondary effects, 444 
types and relative incidence, 440 
in croupous pneumonia, 209 
malignant, 435 

diagnosis, 438 
ulcerative, 435 
Endotheliocytosis in pleural fluid, 54 
Energy index, 36 

Enlargement of lateral thoracic glands, 
116 
of thymus gland, 504 
Enteroptosis, 520 
Enteroptotic abdomen, 520 
Epigastric angle, 75 



INDEX 



5§ 



Epigastric artery, deep, clinical anat- 
omy, 509 

region, 511 
Epigastrium, enlargement of, 522 

pain in, 530 

palpable thrill in, 528 

pulsations in, 332 
Epinephrin test, 404 
Episternal notch, pulsation in, 331 
Erni's sign, 237 
Erythroblastosis, fetal, in 
Essential asthma, 181 
Ether pneumonia, 200 
E wart's paravertebral area, 22 

sign, 411 
Excrescences, beaded, of valves, 435 

verrucose, of valves, 435 
Exercise, effect of, on heart, 363 

test for functional capacity of heart, 
403 
Exocardial murmurs, 397 
Extrasystole, 374 

auricular, 374 

auriculo ventricular, 374 

ventricular, 373 
Exudate in pleural fluid, 53 



Facies, hepatic, 555 

Falciform ligament, 552 

Falling-drop sound, 174 

False aneurism of thoracic aorta, 490 

Fat necrosis of abdomen, 526 

Fecal impaction, 550 

Fetal erythroblastosis, in 

Fetid bronchitis, 179 

Dittrich's plugs in, 1 79 
Fetus, white pneumonia of, 245 
Fibrillation arhythmia, 377 
auricular, 377 
ventricular, 378 
Fibrinous bronchitis, 179 
auscultation in, 180 
bruit de drapeau in, 180 
clinical pathology, 179 
diagnosis, 180 
physical signs, 180 
pericarditis, acute, 405 
pleurisy, 290 
acute, 274 

clinical pathology, 274 
diagnosis, 275 
physical signs, 274 ' 
in croupous pneumonia, 209 
.pneumonia, 203 
Fibroid induration of lung, 219 
lung, 219 
phthisis, 241 



Fibroid phthisis, cicatrices fistuleuses 
in, 241 
clinical pathology, 241 
diagnosis, 244 
physical signs, 242 
pneumonia, 219 
circumscribed, 221 
clinical pathology, 219 
diagnosis, 222 
diffuse, 219 
physical signs, 221 
Fibrosis, myocardial, 429 

of lung, 244 
Fibrotuberculosis of lung, 241 
Finger, clubbed, 123 
drumstick, 123 
percussion, 13 
Fistula sound, pulmonary, 169 
Flack and Keith's node, 321 
Flanks, clinical anatomy, 509 
Flat thorax, 86 
Flatness, 13, 19 
cardiac, area of, 358 
hepatic, 560 
pulmonary, 144, 147 
Flexion-folds, cutaneous, of abdomen, 

509 
Flint murmur, 390 
Floating kidney, 573 
Fluctuation, abdominal, 527 

in diseases of pleura and lungs, 137 
Fluid veins, 382 
Fluroscopy, 67 
Flutter, auricular, 342 
Foramen ovale, patent, 486, 488 
Fossa, Mohrenheim's, 73 
Fourmentin's thoracic index, 72 
Fractional method of sphygmoman- 

ometry, 34 
Fremissement cataire, 335, 455 
Fremitus, friction, 137, 336 

hydatid, 138, 528 

muscular, 138 

rhonchal, 137 

succussion, 137 

tussive, 137 

vocal, 134 
decreased, T36 
increased, 136 
Frictio indux, 283 

redux, 171 
Friction, abdominal, 515 

fremitus, 137, 33° 

intercostal, 172 

pericardial, 336 

peritoneal, 515 
in peritonitis, 528 

pleural, 170 



584 



INDEX 



Friction, pleuropericardial, 172, 336 

shoulder-blade, 172 

shoulder-joint, 172 

tactile, of abdomen, 528 

tubercle, 515 

in tuberculous peritonitis, 528 
Friction-sounds, gall-bladder, 562 

perihepatitis 562 

splenic, 569 
Friedlander's pneumonia, 204 
Friedreich's sign, 153, 331, 416 
Functional capacity of heart, 403 

murmurs, 385 
Funnel-breast, 85 

Funnel-shaped stenosis, mitral, 451 
Furrow, Harrison's, 85 

Sibson's, 75 



Gaxrdxer's coin-test, 154 
Gall-bladder, clinical anatomy, 552 

crepitations, 562 

enlargement of, 561 

examination of, 552 

friction-sounds, 562 

inspection of, 555 

palpation of, 558 

systolic souffle over, 562 
Gall-stone crepitus, 515 

:v-ray examination in, 555 
Gallop rhythm, 370 
Galloping consumption, 222 
Galvanometer, string, Lewis' diagram 

of, 45 
Gangrene, pulmonary, 264 . 

after croupous pneumonia, 209 
circumscribed, 265 
clinical pathology, 264 
diagnosis, 266 
diffuse, 266 
physical signs, 266 
Gas asphyxiation, bradycardia in, 345 

bronchitis, 193, 194 

edema, 193 

mustard, effects of, 200 

pneumonia, 200 
Gaseous abdomen, 519 

pulse, 349 
Gases, suffocating, effects of, 193 
Gassing, asphyxia! stage of, 193 

effects of, 193, 200 

tracheobronchitic stage of, 194 
Gastralgia, pain of, 538 
Gastrectasis, 534 
Gastritis, pain of, 538 
Gastrodiaphany, 537 
Gastroptosis, 534 
Gastroptotic abdomen, 520 



Gerhardt's sign, 154 

Gibson's rule in pneumonia, 211 

Glands, lateral, thoracic, enlargement 

of, 116 
Glandular enlargements about thorax, 

in 
Glasgow's sign in aneurism of thoracic 

aorta, 500 
Glass-blowers' emph} T sema, 249 
Glenard's disease, 520 

method of palpating liver, 557 
Goat-leap pulse, 351 
Goldscheider's method of threshold 

percussion, 14 
Graham Steelle murmur, 495 
Granular myocardial degeneration, 429 
Gray induration of lung, 220 
Grinder's asthma, 259 

rot, 259 _ 
Grocco's sign, 146, 280 

in abdominal cyst, 282 
in ascites, 282 
in lumbar abscess, 282 
in pregnancy, 282 
in serofibrinous pleurisy, 281 
in subphrenic abscess, 282 
Groin, enlarged glands in, 526 
Gurgle, metallic, 400 
Gurgling in stomach, 543 
metallic, in pneumopericardium, 419 
rales, 169 
Gutta cadens, 174 

in pneumothorax, 299 
Gutter-chest, 88 



Hair crepitus, 165 
Hairy heart, 408 
Harrison's furrow, 85 
Hawksley's stethoscope, 26 
Heart, alternation of, 346 

anomalies of size, 487 

apex of, thrill at, 335 

area, displacement of, 363 

athlete's, 462 

atrophy of, 487 

auricles of, clinical anatomy, 317 

auscultation of, 363 

base of, 317 
pulsations at or near, 331 
thrill at, 335 

borders, postural influences on, 360 

clinical anatomy, 318 

compensatory hypertrophy of, 442 

Copenhagen, 450 

cycle, 319 

debility, 406 _ 

decompensation of, 442 



INDEX 



58S 



Heart, dilatation of, 425. See also 
Dilatation, cardiac. 
disease, congenital, 485 
clinical pathology, 485 
physical signs, 487 
disordered action of, 406 
dulness, area of, 359 
decrease in, 362 
increase in, 361 
dyspnea, 105 
effect of exercise on, 363 
flatness, area of, 358 
functional capacity of, 403 
epinephrin test, 404 
exercise test, 403 
pulse pressure test, 404 
hairy, 408 
hypertrophy of, 419, 487. See also 

Hypertrophy, cardiac. 
in gastric cancer, 362 
irritable, 405 
jinrikisha, 462 

malpositions of, congenital, 486 
movements, 320 
orifices of, 318 

ruptured compensation of, 442 
soldier's, 405. See also Soldier's 

heart. 
valves of, 318 
Heart-beat, 319 

myogenic theory, 320 
neurogenic, 320 
Heart-block, 376 
arhythmia, 375 
complete, 375 
incomplete, 375 
sino-auricular, 377 
Stokes-Adams', 375 
Heart-disease cells, 191 
Heart-sounds, 364 
adventitious, 380 
first, 365 

at apex, accentuation of, 367 

enfeeblement of, 368 
reduplication of, 370 
in croupous pneumonia, 213 
intensity of, changes in, 366 
psychic, 386 

quality of, changes in, 367 
reduplication of, 370 
second, 366 

at base, accentuation of, 368 

enfeeblement of, 369 
reduplication of, 371 
third, 365 
Hemisystolic arhythmia, 379 
Hemopericardium, 418 
HemopneumoDericardium, 418 



Hemopneumothorax, 294 
Hemorrhage, concealed, of phthisis, 228 

pericardial, 418 

pleural, 293 
Hemorrhagic infarction of lungs, 193 
clinical pathology, 195 
diagnosis, 197 
physical signs, 197 

pleurisy, 276 
Hemothorax, 293 
Hen-cluck stertor, 101 
Hepatic facies, 555 

flexure, clinical anatomy, 546 
Hepatization, white, of lung, 244 
Hepatoptosis, 561 
Herrick's method of paracentesis in 

diagnosis of pneumoperitoneum, 57 
Hill-Barnard sphygmometer, 35 
Hilus tuberculosis, 229, 240 
Hippocratic succussion sound, 174 
His' bundle, 321 
Hoover's method of inspection and 

palpation of subcostal angle, 96 
Hour-glass stomach, 535 
Huchard's paradoxic percussion sound, 

194 _ 
Humming-top murmur, 402 
Hydatid fremitus, 138 

resonance, 19 

thrill, 528 
Hydronephrotic cysts, examination of 

fluid from, 60 
Hydropericardium, 417 
Hydropneumopericardium, 418 
Hydropneumothorax, 294 
Hydrops adiposus, 276 

chylosus, 276, 294 

ex vacuo, 293 
Hydrothorax, 292 
Hyperemia of lungs, 189 
Hyperresonance in compensatory em- 
physema, 148 

in hypertrophic emphysema, 148 

pulmonary, 147 

pulmonary relaxation as cause, 
148 
Hyperresonant percussion-sounds, 13, 

19 
Hypertension, 36 
Hypertrophy, cardiac, 419, 487 

auricular, 422 

circumscribed, 419 

clinical pathology, 419 

compensatory, 442 

concentric, 419 

diagnosis, 424 

eccentric, 419 

general, 419, 421 



586 



INDEX 



Hypertrophy, cardiac, partial, 419 
physical signs, 422 
primary congenital, 422 
simple, 419 
ventricular, left, 422 
right, 422 
ox-heart, 420 
Hypochondriac region, 79 

pain in, 531 
Hypochondrium, left, pain in, 120 

right, pain in, 119 
Hypogastric region, 511 

pain in, 530 

Hypotension, 36 

in aviators, 36 

in effort syndrome, 461 



Ileocecal valve, clinical anatomy, 545 
Ileolumbar region, pain in, 531 
Ileum, clinical anatomy, 544 
Iliac arteries, common, 509 

region, 511 

spines, anterior superior, 508 
Illness, serum, 53 
Incisura angularis of stomach, clinical 

anatomy, 533 
Incomplete heart-block, 375 
Index, energy, 36 

thoracic, Fourmentin's, 72 
Infarction, hemorrhagic, of lungs, 195. 

See also Hemorrhagic infarction of 

lungs. 
Infiltration, serous, of lungs, 192 
Inflated thorax, 80 
Influenzal pneumonia, 207 
Infra-axillary region, 79 
Infraclavicular region, 79 
Infracostal line, 78, 510 
Inframammary region, 79 
Infrascapular line, 79 

region, 79 
Inguinal region, 511 
Innominate artery, aneurism of, 502 
clinical anatomy, 319 

veins, clinical anatomy, 319 
Inoscopy of pleural fluid, 55 
Inspection, 12 

of abdomen, 512 

of cardiovascular system, 323 

of gall-bladder, 555 

of intestines, 546 

of kidneys, 571 

of liver, 555 

of lungs, 130 

of spleen, 564 

of stomach, 533 
Instrumental percussion, 13 



Intensity of sound, 18 
Intercostal spaces as landmarks of 
thorax, 74 
pulsations in, 331 
thrill at, 335 
Interscapular area, impairment in, 
dulness from, 147 
region, 79 
Interspinal line, 510 
Interstitial pneumonia, chronic, 219. 

See also Fibroid pneumonia. 
Interventricular groove, clinical anat- 
omy, 318 
septum, defects of, 485, 487 
Intestinal obstruction, 547 

sounds, 515 
Intestines, clinical anatomy, 544 
examination of, 544 
inspection of, 546 
large, clinical anatomy, 545 
x-ray examination of, 546 
malignant disease, 551 
palpation of, 546 
percussion of, 551 
peristalsis of, 524 
small, clinical anatomy, 544 
percussion of, 551 
ptosis of, 549 
Intradural pressure in lumbar punc- 
ture, 62 
Irregular pulse, perpetually, 346 
Irritable heart, 405 
Isthmus, Kronig's, 144, 236 



Jaquet's sphygmocardiograph, 38 

Jejunum, clinical anatomy, 544 

Jinrikisha heart, 462 

Joint, xiphisternal, 73 

Jug sound, 150 

Jugular veins, diastolic collapse, 331 

engorgement, 334 

pulsations, 330 
Jiirgensen's sign in acute broncho- 
pneumonic phthisis, 224 



Kaolinosis, 260 

Katzenschurren, 335 

Keel breast, 84 

Keith and Flack's node, 321 

Kent's node, 321 

Kidneys, clinical anatomy, 570 

enlarged, 573 

examination of, 570 

floating, 573 

inspection of, 571 

movable, 572 



INDEX 



587 



Kidneys, palpable, 572 

palpation of, 572 

percussion of, 573 

puncture of, 66 
Kilgore's fractional method of sphyg- 

momanometry, 34 
Knife-grinder's phthisis, 259 
Koch's tuberculin test, 68 
Koranyi's method of percussion, 17 

spinal zones, 21 
Kronig's isthmus, 144, 236 
Kussmaul's air-hunger, 104 

sign, 334, 416 
Kyphosis, 84 



Laennec's catarrhe pituiteux, 179 
sec, 179 

perles in bronchial asthma, 182 

theory of vesicular breathing, 157 
Landon's spinal manometer, 63 
Laryngeal crepitus in phthisis, 239 

paralysis in mitral stenosis, 454 

rales, 166 
Larynx, displacement of, 131 
Law, Courvoisier's, 561 
Leaden overcast, 324 
Leopard's growl, 102 
Lewis' diagram of string galvanom- 
eter, 45 
Lian's point, 58 
Ligament, falciform, 552 
Ligaments, Poupart's, 508 
Ligne blanche abdominale, 526 
Line, axillary, anterior, 76 
posterior, 76 

clavicular, 76 

costal, third, 76 
sixth, 78 

cricoclavicular, 76 

Ellis', in serofibrinous pleurisy, 280 

infracostal, 78, 510 

infrascapular, 79 

interspinal, 510 

mammillary, 76 

midaxillary, 76 

midclavicular, 76 

midsternal, 76 

of costal arch, 78 

of transmission of murmurs, 383 

of twelfth thoracic vertebra, 79 

parasternal, 76 

Poupart's, 510 

scapular, 76 
spinal, 79 

sternal, 76 
Linea alba, 509 

albicantes, 526 



Linea gravidarum, 526 

nigra, 509 
Lineae semilunares, 509 

transversa?, 509 
Lithosis, 259 
Litten's sign, 95 
Liver, areas of dulness and flatnees, 558 

auscultation of, 562 

clinical anatomy, 552 

consistence of, 557 

contour of, 557 

corset-, 558 

decrease in size of, 560 

descent of, 556 

displacement of, 561 

enlargement of, 556, 560 

examination of, 552 

inspection of, 555 

pain in region of, 555 

palpation of, Glenard's method, 557 

percussion of, 558 

prolapse of, 561 

pulsations of, 332, 555 

puncture of, 66 

surface topography, 553 

tenderness in region of, 555 

venous bruit over, 562 
murmur over, 562 
Lobar atelectasis, 259 

pneumonia, 203 
Lobular pneumonia, 197 
Locomotive pulse in aortic regurgita- 
tion, 464 
Loin, clinical anatomy, 509 

pain in, 531 
Lombardi's sign of apical phthisis, 232 
Lordosis, 84 
Lorenz's sign in chronic ulcerative 

phthisis, 230 
Louis' angle, 73 

pulsations in, 331 
Lumbar muscle spasm, 572 

puncture, 60 

region, 511 
pain in, 122 
Lungs, abscess of, 262. See also 
Abscess of lung. 

actinomycosis of, 271 
physical signs, 271 

albinism of, 244 

alveolar ectasia, 248 

anterior borders, 125, 126 

apices of, 125 
expansion of, 133 

Bethea's method of determining, 

W . , 

Kronig s isthmus, 144 

pain at, 119 



5%8 



INDEX 



Lungs, apices of, percussion of, 138 
apoplexy of, 192, 195 
atrophy of, senile, 253 
auscultation of, 155 
bases of, relative expansion of, 133 
borders of, changes in mobility and 
position, 143 

lower, 142 

normal limits, 142 

upper, 142 
brown induration, 190 
carcinoma of, 267 

physical signs, 269 
carnification of, 257 
catarrhal pneumonia, 197 
cavities of, tympany in, 149 
circulation of, 322 
cirrhosis of, 219 

after croupous pneumonia, 209 
clinical anatomy, 124 
coal-miner's, 259 
collapse of, 255 
congestion of, 189 

acute, 189, 191 

chronic, 190, 191 

clinical pathology, 189 

collateral, 190 

diagnosis, 192 

hypostatic, 190, 192 

mechanical, 190 

passive, 190 

physical signs, 191 
costal surfaces, 124 
croupous pneumonia, 203 
dilatation of, acute, 254 
dropsy of, 192 
dulness of, 144. See also Dulness of 

lung. 
dyspnea of, 105 
echinococcus cyst, 272 
edema of, 192. See also Edema of 

lungs. 
emphysema of, 247. See also Em- 
physema, pulmonary. 
fever, 203 
fibroid, 219 

induration, 219 
fibrosis of, 244 
fissures of, 127 
fistula sound, 169 
flatness of, 144 
gangrene of, 264. See also Gangrene, 

pulmonary. 
gray induration, 220 
hemorrhagic infarction, 195. See 

also Hemorrhagic infarction of 

lungs. 
hilus of, 125 



Lungs, hyperemia of, 189 
inspection of, 130 
lobes of, 127 

limits, 127 
lower borders, 126 
mediastinal surfaces, 124 
mobility of, gaging, by pulmonary 

borders, 143 
palpation of, 132 
percussion of, 138 

comparative, 139 
potter's, 260 
puncture of, 66 
reflex, 155 
root of, 125 
sarcoma of, 270 
sclerosis of, 219 
senile atrophy, 253 
serous infiltration, 192 
syphilis of, 244. See also Syphilis, 

pulmonary. 
tuberculofibrosis of, 241 
tumors of, 267 
tympany of, 147 
white hepatization, 244 
Lymphadenitis, mediastinal, 306 

physical signs, 306 

simple, 306 

Smith's murmur in, 308 

suppurative, 306 
Lymphocytosis in pleural fluid, 54 



Mal d'Aviateur, 36 
Malignant endocarditis, 435 

diagnosis, 438 
Mammary region, 79 

veins, enlarged, 107 
Mammillary line, 76 
Manometer, spinal, Landon's, 63 
McBurney's point, 531 
Mediastinal lymphadenitis, 306 
physical signs, 306 
simple, 306 

Smith's murmur in, 308 
suppurative, 306 

pleurisy, 290 
Mediastinitis, 303 

acute, 303 

chronic, 303 

suppurative, 304 
Mediastinopericarditis, 414 

indurative, 303 
Mediastinum, anterior, 130 

clinical anatomy, 129 

diseases of, 175 

middle, 130 

posterior, 130 



INDEX 



539 



Mediastinum, superior, 130 

tumors of, 309. See also Tumors of 

mediastinum. 
Meningeal respiration, 101 
Mensuration of abdomen, 514 

of thorax, 29 
Mesocardia, 486 
Metallic gurglej 400 

in pneumopericardium, 419 
tinkling, 174 
Micrococcus Pasteuri, 204 
Midaxillary line, 76 
Midclavicular line, 76 
Midspinal line, 76 
Midsternal line, 76 

Milk-spots in serofibrinous pericar- 
ditis, 410 
Mirror-image of precordial region, 326 
Mitral area, 364 
murmurs, 390 

presystolic, 390 

systolic, 391 
regurgitation, 446 

clinical pathology, 446 

diagnosis, 450 

muscular type, 447 

organic type, 446 

physical signs, 448 

pulmonary pulse in, 448 

radial pulse in, 449 
stenosis, 451 

clinical pathology, 451 

Corrigan's button-hole mitral de- 
fect in, 451 

diagnosis, 460 

first stage of, 456 

fremissement cataire in, 455 

funnel-shaped, 451 

physical signs, 455 

pulse in, 455 

recurrent laryngeal nerve paral- 
ysis in, 454 

relative, 453 

Samson's double shock sound 
in, 456 

second stage of, 458 

soft-valve, 453 

third stage of, 459 
valve, clinical anatomy, 318 
Mobile cecum, 549 

physical signs, 549 
Mohrenheim's fossa, 73 
Moist rales, 167 
Money-chink resonance, 151 
Moro's reaction, 71 
Morris' point, pain at, 530 
Mortification, pulmonary, 264 
Mouneret's pulse, 349 



Mountain sickness, 103 
Mouse-tail pulse. 
Movable kidney, 572 

pulse in aortic regurgitation, 464 
Mucous catarrh, 179 

click, 168 

rales, 169 
Multiple murmurs, 396 
Munro's point, 58 
Murmurs. See also Bruit. 

analysis of, 388 

anemic, 393 
diastolic, 393 

aortic, 387, 392 
diastolic, 392 
systolic, 392 

arterial, 400 
diastolic, 401 
systolic, 400 

cardiorespiratory, 399 

clinical attributes, 382 

deglutition, of stomach, 543 

diastolic, 383 

Duroziez's, 401 

endocardial, 381 

exocardial, 397 

Flint, 390 

functional, 385 

Graham Steelle, 485 

humming-top, 402 

intensity and quality, 383 

line of transmission, 383 

mid-diastolic, 383 

mitral, 390 

presystolic, 390 
systolic, 391 

multiple, 396 

of high pressure in pulmonary artery, 

485. 

organic, 381 

pericardial, 397 

intensity and quality, 398 
rhythm of, 398 

pericarditic, presystolic, 391 

point of maximum intensity, 383 

post-systolic, 383 

protodiastolic, 383 

psychic heart, 386 

pulmonic, diastolic, 396 
systolic, 395 

rhythm of, 383 

Rogers', 487 

safety-valve, 387 

see-saw, in aortic regurgitation, 468 

Smith's, in mediastinal lymphaden- 
itis, 308 

Snellen's, 403 

systolic, 383 



59° 



INDEX 



Murmurs, systolic, apical, 386 
pulmonic, 386 
. tricuspid, 386 
transmission of, 383 
tricuspid, 393 
presystolic, 393 
systolic, 393 
vascular, 400 
venous, 402 

over hepatic area, 562 
Muscle sounds, 165 

spasm, lumbar, 572 
Muscular atrophy, progressive, thorax 
of, 88 
fremitus, 138 
rigidity of abdomen, 527 
Musset's sign in aortic regurgitation, 

464 
Mustard gas, effects of, 200 
Mute pneumothorax, 300 
Myocardial abscess, 429 
degeneration, granular, 429 
fibrosis, 429 
Myocarditis, 429 
acute, 429 

interstitial, 430 
parenchymatous, 429 
suppurative, 430 
chronic, 430 
clinical pathology, 429 
diagnosis, 432 

in croupous pneumonia, 209 
physical signs, 432 
Myoidema in phthisis, 237 

Naunyn's sign, 530 
Navel, 509 

condition of, 526 
Neck, pulsations in, 330 

venous suffusion, 131 
Necropneumonia, 264 
Necrosis, fat, of abdomen, 526 
Nephroptosis, 572 
Neurocirculatory asthenia, 406 
Neuroses, functional, as cause of 

functional dyspnea, 103 
Nicholson's sphygmomanometer, 31 
Nipple as landmark of thorax, 75 
Nodal rhythm, 374, 377 
Node, auriculo ventricular, 321 

Keith and Flack's, 321 

Kent's, 321 

sino-auricular, 321 

Tawara's, 321 
Nodules, Aschoff's, 431 

subcutaneous, of abdomen, 526 
Noise, water-whistle, 169 
in pneumothorax, 299 



Obese abdomen, 516 
Obturation atelectasis, 187 
Occipital glands, enlargement, 112 
Oculocardiac reflex, 345 
Oligopnea, 99 

Oliver's method of estimating venous 
pressure, 37 

sign, 336 
Ophthalmoreaction, Calmette's, 70 
Organ-pipe arrangement of intestinal 

loops, 548 
Organic murmurs, 381 
Orthopnea, 102 
Osteal resonance, 19 
Ovarian cysts, examination of fluid 

from, 59 
Ox-heart hypertrophy, 420 



Pain at apex of lungs, 119 

at Morris' point, 530 

at Robson's point, 530 

gastric, 538 

in abdomen, 528 

in breast, 119 

in cancer of stomach, 538 

in coccygeal region, 123 

in costal arch, 121 

in epigastrium, 530 

in hepatic region, 555 

in hypochondriac region, 531 

in hypogastric region, 530 

in ileolumbar region, 531 

in lateral wall of thorax, 121 

in left hypochondrium, 1 20 
shoulder, 119 

in loins, 531 

in lumbar region, 122 

in posterior wall of thorax, 121 

in precordia, 119 

in right hypochondrium, 119 
shoulder, 119 

in sacral region, 1 23 

in sacrum, 531 

in splenic region, 566 

in thorax, 119 

in tumors of stomach, 538 

in umbilical region, 530 

of gastralgia, 538 

of gastric ulcer, 538 

of gastritis, 538 

sternal, 119 
Palpable kidney, 572 
Palpation, 12 

of abdomen, 513 

of cardiovascular system, 323 

of gall-bladder, 558 

of intestines, 546 



INDEX 



591 



Palpation of kidneys, 572 

of liver, Glenard's method, 557 

of lungs, 132 

of spleen, 564 

of stomach, 537 
Palpatory percussion, 15 
Pancarditis, 435 
Pancreas, clinical anatomy, 562 

cysts of, examination of fluid from, 

60 . 
physical examination, 562 

Parabronchial consolidations, tym- 
pany from, 150 
Paracentesis, 47 

abdominis, 56 

Buth's method, 58 
diagnostic, 56 
therapeutic, 58 

Herrick's method of, in diagnosis of 
pneumoperitoneum, 57 

lumbar, 60 

of kidney, 66 

of liver, 66 

of lung, 66 

of pericardial sac, 55 

of pleural cavity, 50 

of spleen, 65 

technic, 47 

visceral, 65 
Paralytic thorax, 80 
Parasternal dulness, 147 

line, 76 
Paravertebral dulness, 147 
Paresis, cardiosplanchnic, 406 
Parietal pleura, 1 28 
Parotid gland, enlargement, 115 
Paroxysmal dyspnea, 102 

tachycardia, 343 
Patency of ductus arteriosus, 485, 487 
Patent foramen ovale, 486, 488 
Pectoriloquy, 163 

whispering, 163 
Pectus carinatum, 84 

excavatum, 85 
Pendulum rhythm, 380 
Percussion, 12 

auscultatory, 15 
of stomach, 542 

finger, 13 

immediate, 13, 14 

in intestinal obstruction, 552 

instrumental, 13 

Koranyi's method, 17 

mediate, 13 

of abdomen, 514 

of anterior chest- wall, 138 

of apices of lungs, 138 

of back, 138 



Percussion of cardiovascular system, 
358 
methods and technic, 360 

of colon, 551 

of intestines, 551 

of kidneys, 573 

of lateral regions of thorax, 138 

of liver, 558 

of lungs, 138 

comparative, 139 

of small intestine, 551 

of spleen, 567 

of stomach, 541 

palpatory, 15 

respiratory, 139 

sense of resistance, 17, 18 

spinal, 20 

technic, 13 

threshold, Goldscheider's method, 14 

zones, spinal, 21 
Percussion-sound, attributes, 17 

duration, 18 

Huchard's, 194 

hyperresonant, 13, 19 

intensity, 18 

pitch, 17 

quality, 17 

resonant, 13, 18 

special tonal changes of, 151 

tonal properties, 18 

tympanic, 13, 19 
Perez's sign, 172 
Perforation of stomach, metallic rub in, 

543 
Peribronchial pneumonia, 197 
Pericardial abscess, 413 
dropsy, 417 
effusion, serous, 410 
fluid, examination, 56 
friction, 336, 397 

intensity and quality, 398 
rhythm of, 398 
hemorrhage, 418 
sac, puncture of, 55 
succussion sounds, 400 
Pericardicentesis, 55 
Pericarditic presystolic rumble, 391 

pseudocirrhosis, 304 
Pericarditis, 405 
adhesive, chronic, 414. See also 

Adhesive pericarditis, chronic. 
external, 304 
fibrinous, acute, 405 

clinical pathology, 405 
diagnosis, 409 
physical signs, 408 
in croupous pneumonia, 209 
internal, 304 



592 



INDEX 



Pericarditis, plastic, acute, 405 
purulent, 413 

clinical pathology, 413 

physical signs, 414 
serofibrinous, 410 

Auenbrugger's sign in, 411 

clinical pathology, 410 

diagnosis, 412 

Ewart's sign in, 411 

milk-spots in, 410 

physical signs, 410 

Rotch's sign in, 411 
Pericardium, adherent, 414 

empyema of, 413 
Pericolitis sinistra, 550 
Perihepatitic friction-sound, 562 
Peristalsis of stomach and intestine, 

5?4 
Peristaltic unrest, 525 
Peritoneal friction, 515 
in peritonitis, 528 
Perpetually irregular pulse, 346 
Phonometry, 28 
Phonophore, Arnold's, 26 
Phthisical thorax, 80 
Phthisis, acute bronchopneumonia 223 
Jiirgensen's sign in, 224 
physical signs, 224 
pneumonic, 222 

clinical pathology, 222 
diagnosis, 225 
physical signs, 224 
after croupous pneumonia, 209 
aneurismal, 504 
apical, Lombardi's sign, 232 
black, 259 
chronic ulcerative, 226 

chloasma phthisicorum in, 232 
clinical pathology, 226 
concealed hemorrhage of, 228 
diagnosis, 239 
laryngeal crepitus in, 239 
Lorenz's sign in, 230 
myoidema in, 237 
periods of, 230 
physical signs, 230 
Rothschild's sign in, 230 
signe du tapotage in, 237 
striae vasculares in, 232 
valvular heart disease in, 228 
Williams' sign in, 233 
fibroid, 241. See also Fibroid 

phthisis. 
fiorida, 222 
galloping, 222 
knife-grinder's, 259 
Sabourin's sign, 232 
slow, 226 



Phthisis, stone-cutter's, 259 

Physical diagnosis, methods and tech- 

nic, n 
Physiologic venous pulse, 42 
Pick's disease, 304 
Pigeon-breast, 84 
Pirquet's tuberculin test, 69 
Pistol pulse in aortic regurgitation, 466 
Pitch of sound, 17 
Pitres' signe du sou, 155 
Plastic bronchitis, 179 
pericarditis, acute, 405 
pleurisy, 274 
chronic, 290 
Pleura, carcinoma of, 302 
clinical anatomy, 128 
parietal, 128 
sarcoma of, 303 
rumors of, 302 
visceral, 128 
Pleural cavity, puncture, 50 
dropsy, 292 

fluid, cancer cells in, 54 
cytodiagnosis, 54 
endotheliocytosis in, 54 
examination, 53 
exudate in, 53 
inoscopy of, 55 
lymphocytosis in, 54 
polynucleosis in, 54 
transudate in, 53 
friction, 170 
hemorrhage, 293 
space, complementary, 129 
Pleuresie bloquee, 51 
Pleurisy, 273 
acute dry, 274 
adhesive, chronic, 290. See also 

Adhesive pleurisy, chronic. 
blocked, 51 
chyliform, 276 
circumscribed, 288 
diaphragmatic, 288 
encapsulated, 289 
encysted, 289 
fibrinous, 290 
acute, 274. See also Fibrinous 

pleurisy, acute. 
in croupous pneumonia, 209 
hemorrhagic, 276 
interlobar, 289 
mediastinal, 290 
plastic, 274 

chronic, 286 
pulsating, 286 

purulent, 285. See also Empyema. 
serofibrinous, 275. See also Sero- 
fibrinous pleurisy. 



INDEX 



596 



Pleurisy with effusion, 275 
Pleuritis, 273 

sicca, 274 _ 
Pleurocentesis, 50 
Pleuropericardial friction, 172, 336 
Pleuropneumonia, 209 
Pneumochysis, 192 
Pneumonia, apex, 204 

aspiration, 200 

catarrhal, 197. See also Catarrhal 
pneumonia. 

central, 205 

contusion, 216 

core, 205 

crossed, 204 

croupous, 203. See also Croupous 
pneumonia. 

deglutition, 200 

disseminated, 197 

double, 204 

embolic, 195 

errans, 205 

ether, 200 

fibrinous, 203 

fibroid, 219. See also Fibroid pneu- 
monia. 

Friedlander, 204 

gas, 200 

Gibson's rule in, 211 

hypostatic, 191 

influenzal, 207 

interstitial, chronic, 219. See also 
Fibroid pneumonia. 

lobar, 203 

lobular, 197 

massive, 205 

migrans, 205 

peribronchial, 197 

purulent, 262 

stripe, 205 

superficial, 205 

syphilitic, 244 

toxic, 214 

traumatic, 216 

typhoid, 214 

wandering, 205 

white, 244 
of fetus, 245 
Pneumonic phthisis, acute. See also 

Phthisis, acute pneumonic. 
Pneumonitis, 203 
Pneumonoconiosis, 259 

clinical pathology, 259 

diagnosis, 262 

physical signs, 262 
Pneumopericardium, 418 

bruit de moulin in, 419 

metallic gurgling in, 419 

38 



Pneumopericardium, physical - 

418 
Pneumoperitoneum, 520 

diagnosis of, Herrick's method of 
paracentesis in, 57 
Pneumorrhagia, 195 
Pneumothorax, 294 

artificial, 53 

bilateral, 296 

bruit d'airain in, 299 

circumscribed or limited, 296 

clinical pathology, 294 

closed, 296 

diagnosis, 299 

general or complete, 296 

gutta cadens in, 299 

mute, 300 

open, 296 

physical signs, 297 

succussio Hippocratis in, 299 

tympany in, 150 

valvular, 296 

ventilated, 296 

water-whistle noise in, 299 
Pneumotyphus, 214 
Point, Clado's, 531 

Lian's, 58 

McBurney's, 531 

Morris', 530 

Munro's, 58 

Robson's, 530 

spleen, 566 

Voillemier's, 531 
Polynucleosis in pleural fluid, 54 
Polypnea, 99 

Polypous lesions of valves, 435 
Posture, influence, on cardiac signs, 324 
on percussion sound, 142 
on precordial borders, 360 
on vocal fremitus, 134 
Potain's aspirator, 49 
Potassium content of cerebrospinal 

fluid, 64 
Potter's lung, 260 
Poupart's ligaments, 508 

lines, 510 
Precordia, bulging of, 324 

clinical anatomy, 3 1 7 

flattening or depression of, 325 

pain in, 119 
Precordial area, pulsations in, 331 

contour, 324 
Pregnancy, abdomen of, 517 
Progressive muscular atrophy, thorax 

of, 88 
Prolapse of liver, 561 
Pseudo-alternation of pulse, 37 
Pseudocirrhosis, pericarditic, 304 



594 



INDEX 



Pseudolipoma, Verneuil's, 92 
Psychic heart murmur, 386 
Pterygoid thorax, 80 
Ptosis of small intestine, 549 
Pubic region, 511 

spines, 508 

symphysis, 508 
Puff, veiled, Laennec's, 159 
Pulmonary artery, aneurism of, 502 
clinical anatomy, 319 
transposition of, 487 

edema, 192 

pulse in mitral regurgitation, 448 

regurgitation, 483. See also Regur- 
gitation, pulmonary. 

resonance, 139. See also Resonance, 
pulmonary. 

splenization, 191 

stenosis, 479. See also Stenosis, 
pulmonary. 

tympanites, 147-149 
Pulmonic area, 364 

murmurs, diastolic, 396 
systolic, 386, 395 

sound, second, accentuation of, 368 
weakening of, 370 

valve, clinical anatomy, 318 
Pulsating empyema, 286 

pleurisy, 286 
Pulsations, abnormal areas of, 3 29 

at Louis' angle, 331 

at or near base of heart, 331 

carotid, 330 

circumscribed areas of, in diseases 
of lungs and pleura, 131 

in epigastrium, 332 
postsystolic, 332 
systolic, 332 

in episternal notch, 331 

in intercostal spaces, 331 

in neck, 330 

in precordial area, 331 

of jugular veins, 330 

of liver, 332, 555 

of spleen, 566 

under outer half of left clavicle, 330 
Pulse, allorhythmic, 346 

alternating, 346, 378 

arachnoid, 352 

arterial, 336 

asymmetry of, 353 

bigeminal, 346 

capillary, 353, 465 

caprizant, 351 

collapsing, 466 

Corrigan's, 466 

decurtate, 352 

feeling, technic of, 337 



Pulse, gaseous, 349 
goat-leap, 351 
hyperdicrotic, 350 
hypertension of, 349, 351 
hypotension of, 349, 351 
in aneurism of abdominal aorta, 505 

of thoracic aorta, 498 
in aortic regurgitation, 466 

stenosis, 472 
in croupous pneumonia, 211 
in edema of lungs, 193 
in mitral stenosis, 455 
in pulmonary regurgitation, 484 

stenosis, 480 
in tricuspid regurgitation, 476 

stenosis, 478 
intermission of, 345 
irregularity of, 345 
locomotive, 464 
Mouneret's 349 
mouse-tail, 352 
movable, 464 
perpetually irregular, 346 
pistol, 466 
pressure, 33 

test for functional capacity of 
heart, 404 
pseudo-alternation of, 37 
pulmonary, 448 
receding, 466 
rhythm of, 337 
tension of, variations in, 347 
velocity of, variations in, 352 
venous, 354. See also Venous pulse. 
volume of, 338 

variations, 347 
water-hammer, 466 
Pulse-rate, 337 

disturbances of, 340 
Pulsus alternans, 346, 378 

sphygmomanometer in study of, 
36 
altus et celer in aortic regurgitation, 

466 
anacrotic, 350 
bigeminus, 346 
bisferiens, 350 

in aortic stenosis, 472 
celer, 352 

celerity of, variations in, 352 
celerrimus, 352 

in aortic regurgitation, 466 
deficiens, 346 
dicroticus, 350 
durus, 349 
equalis, 351 
frequens, 341 
inequalis, 351 



INDEX 



595 



Pulsus inequalis periodicus, 346 

intercidens, 346 

intermittens, 346 

irregularis perpetuus, 377 

magnus, 351 

mollis, 349 

paradoxus, 346 

parvus, 351 

plenus, 351 

rarus, 344 

subungualis, 353 

tardus, 352 

in aortic stenosis, 472 

trigeminus, 346 

vacuus, 352 
Punctum maximum of murmurs, 383 
Puncture, 47. See also Paracentesis. 
Pupils, inequality of, in diseases of lungs 

and pleura, 131 
Purulent pericarditis, 413 

pleurisy, 285. See also Empyema. 

pneumonia, 262 
Putrid bronchitis, 179 
Pylorus, clinical anatomy, 531 
Pyopericardium, 413 
Pyopneumopericardium, 418 
Pyopneumothorax, 294 

subphrenic, 301 
Pyothorax, 285 



Rachitic rosary, 84 

thorax, 83 
Radial sphygmogram, 338 
Radiography, 67 
Rales, 166 

atelectatic, 168 

bronchial, 166 

buccal, 166 

cardiopneumatic, 170 

cavernous, 166 

consonating, 213 
- crepitant, 167 

dry, 166 

emphysematous, 167 

gurgling, 169 

hair, 165 

indux, 168 

laryngeal, 166 
in phthisis, 239 

moist, 167 

mucous, 168 

redux, 168 

in croupous pneumonia, 212 

sibilant, 166 



sonorous, 166 
subcrepitant, 168 
subpleural, 172 



Rales, tracheal, 166 
vesicular, 166 

Rasmussen's aneurism in chronic ul- 
cerative tuberculosis, 
Reaction, atropin, in cardiac compe- 
tency, 341 
Moro's, 71 
tuberculin, 68 
Receding pulse in aortic regurgitation, 

466 
Rectum, clinical anatomy, 546 
Recurrent laryngeal nerve paralysis in 

mitral stenosis, 454 
Reflex, lung, 155 
oculocardiac, 345 
renal, 572 
Reflexes, vertebral, 22 
Regurgitation, aortic, 461. See also 
Aortic regurgitation. 
mitral, 446. See also Mitral regur- 
gitation. 
pulmonary, 483 

clinical pathology, 483 
diagnosis, 485 
organic, 483 
physical signs, 484 
pulse in, 484 
relative, 484 
safety-valve, 447, 475 
tricuspid, 474. See also Tricuspid 
regurgitation. 
Renal asthma, 104 

reflex, 572 
Resistance, increased, in diseases of 

lungs and pleura, 137 
Resonance, amphoric, 150 

band-box, in hypertrophic emphy- 
sema of lungs, 251 
cracked-pot, 151 
hydatid, 19 
impaired, 19 
jug, 150 

money-chink, 151 
osteal, 19 
pulmonary, 139 
anteriorly, 141 
exaggeration of, 147. See also 

Hyperresonance, pulmonary. 
extent of, 143 
laterally, 142 
posteriorly, 142 
regional differences in, 140 
skodaic, 149 
vesicular, 139. See also Resonance. 

pulmonary. 
vesiculotympanitic, 148 
vocal, 163 
Resonant percussion-sounds, 13, 18 



59^ 



INDEX 



Respiration, 94, 156 

abdominal, 95, 96 

absent, 162 

amphoric, 158 

anomalies of, 97 

Biot's, 101 

bronchial, 157 

bronchocavernous, 158 

bronchovesicular, 156, 159 

cavernous, 158 

Cheyne-Stokes', 99 

cog-wheel, 162 

costal, 95, 97 

diaphragmatic, 95 

difficult, 102. See aiso Dyspnea. 

exaggerated, 160 

feeble, 161 

frequency, alterations in, 99 

harsh, 160 

prolonged, 160 

interrupted, 162 

irregularity, 99 

jerky, 99 

meningeal, 101 

normal, 94 

puerile, 160 

rapid, 99 

Seitz's metamorphosing, 159 

senile, 161 

slow, 99 

sternomastoid, 97 

stertorous, 101 

stridulous, 101 

thoracic, 95 

type, 95 

reversal, of 97 

vesicular, 156 

vesiculocavernous, 158 
Respiratory alterations of subcostal 
angle, 96 

arhythmia, 99, 372 

cycle, 94 

movements of thorax, 94. See also 
Respiration. 

percussion, 139 

sounds, 156 

turgescence of cervical veins, 131 
Retraction, abnormal areas of, 332 
Rhonchal fremitus, 137 
Rhonchus, 166 
Rhythm, canter, 370 

gallop, 370 

nodal, 374, 377 

pendulum, 380 
Rib, cervical, pressure of, on sub- 
clavian artery, 504 
Ribs as landmarks of chest, 74, 75 
Riedel's lobe, 558 



Riviere's sign, 240 
Robson's point, pain at, 530 
Rod auscultation, 16 
Rogers' murmur, 487 
Rontgen rays, examination by means 
of, 67 e 
in aneurism, 496 
in chronic interstitial pneu- 
monia, 222 
in croupous pneumonia, 211 
in gall-stones, 555 
in gastric cancer, 537 
diseases, 536 
ulcer, 537 
in mediastinal lymphadenitis, 
308 
neoplasm, 314 
in phthisis, 234 
in pleural effusion, 278 
in pneumothorax, 297 
of large intestine, 546 
Rosary, rachitic, 84 
Rotch's sign, 411 
Rothschild's sign in phthisis, 230 
Ruptured compensation of heart, 442 



Sabourin's sign of apical phthisis, 232 
Saccular aneurism of thoracic aorta, 

Sacral region, pain in, 123 

triangle, 509 
Sacrum, pain in, 531 
Safety-valve murmur, 387 

regurgitation, 447, 475 
Sahli's theory of vesicular breathing, 

i57 
Sander's sign, 416 
Sansom's double shock sound, 457 

leaden overcast, 324 

sign in aneurism of thoracic aorta, 
500 

stethoscope, 25 
Sarcoma of lungs, 270 

of pleura, 303 
Scaphoid abdomen, 516 

scapula, 75 
Scapula, alar, 80 

scaphoid, 75 

winged, 80 
Scapular line, 76 
spinal, 79 

region, 79 
Scars of thorax, 123 

on skin of abdomen, 526 
Schusterbrust, 86 
Sclerosis of lung, 219 
Scoliosis, 84 



INDEX 



597 



Scorbiculus cordis, 73, 508 
See-saw murmur in aortic regurgita- 
tion, 468 
Seitz's metamorphosing respiration, 

159 
Semilunar space, Traube's, 542 
Senile atrophy of lungs, 253 

respiration, 161 
Septum, absence of, between auricles 
and ventricles, 486 

interventricular, defects of, 485, 487 
Serofibrinous pericarditis, 410. See 
also Pericarditis, serofibrinous. 

pleurisy, 275 

Bacelli's sign in, 282 
clinical pathology, 275 
diagnosis, 283 
Ellis' line in, 280 
Grocco's sign in, 280 
physical signs, 277 
Serum illness, 53 
Shoulder, pain in, 119 
Shoulder-blade friction, 172 
Shoulder- joint friction, 172 
Shulman's sign, 523 
Sibilant rales, 166 
Sibson's furrow, 75 

notch, 412 
Siderosis, 259 

Sigmoid flexure, clinical anatomy, 546 
Sign, Auenbrugger's, 411 

Bacelli's, 164, 282 

Bassler's, 550 

Bastedo's, 550 

Biermer's, 154 

Broadbent's, 2>2> 2 i 4*6 

Bryson's, 98 

Drummond's, 500 

Duroziez's, 402, 469 

Erni's, 237 

d'Espine's, 308 

E wart's, 411 

Friedreich's, 153, 331, 416 

Gerhardt's, 154 

Glasgow's, 500 

Grocco's, 147, 280 

Jurgensen's, 224 

Kussmaul's, 334, 416 

Litten's, 95 

Lombardi's, 232 

Lorenz's, 230 

Musset's, 464 

Naunyn's, 530 

Oliver's, 336 

Perez's, 172 

Riviere's, 240 

Rotch's, 411 

Rothschild's, 230 



Sign, Sabourin's, 232 
Sander's, 416 
Sansom's, 500 
Shulman's, 523 
Skoda's, 149 
Stiller's, 539 
Traube's, 469 
Turrettini's, 409 
Williams', 233 
Wintrich's, 151 
Signe du sou, 155 

du tapotage, 237 
Sino-auricular heart-block, 377 
node of Keith and Flack, 321 
Sinus arhythmia, 372 

in effort syndrome, 407 
Situs viscerum inversus, 486 
Skin of abdomen, 525 
Skodaic resonance, 149 
Slow consumption, 226 
Smith's murmur in mediastinal lym- 
phadenitis, 308 
Snellen's murmur, 403 
Snoring, 101 

Soft-valve mitral stenosis, 453 
Soldier's heart, 405 

auscultation in, 407 
clinical pathology, 406 
diagnosis, 407 
inspection in, 406 
organic disease and, differentia- 
tion, 408 
palpation in, 406 
percussion in, 407 
physical signs, 406 
Sonorous rales, 166 
Souffle. See Bruit. 
Sounds, adventitious, 164 
cardiac, 364. See also Heart-sounds. 
extraneous, 165 
falling-drop, 174 
Huchard's percussion, 194 
intestinal, 515 
metallic, 174 
muscle, 165 
pulmonary fistula, 169 
respiratory, 156 
splashing, 173 
stomach, 515 
succussion, 173 
Hippocratic, 174 
of stomach, 539 
Spasm, lumbar muscle, 572 
Spasmodic asthma, 181 
Spens' syndrome, 367 
Sphacelation, pulmonary, 264 
Sphygmocardiogram, interpretation of, 

4i 



598 



INDEX 



Sphygmocardiograph, Jacquet's, 38 
Sphygmocardiography, clinical value 
of, 43 

technic of, 38 
Sphygmogram, arterial, 40, 338 

clinical significance, 338 ' 

radial, 338 

venous, 42 
Sphygmograph, Dudgeon's, 40 
Sphygmography, 37 
Sphygmomanometer, 35 

in study of pulsus alternans, 36 

Nicholson's, 31 

Rogers', 34 
Sphygmomanometry, 31 

auscultatory method, S3 

fractional method, 34 

Kilgore's method, 34 

technic, 31 
Sphygmometer, Hill-Barnard, 35 
Spinal fluid, composition of, 64 

manometer, Landon's, 63 

percussion, 20 

scapular line, 79 

zones, Koranyi's, 21 
Spine, iliac, anterior superior, 508 

pubic, 508 
Splashing sounds, 173 
Spleen, auscultation of, 569 

clinical anatomy, 563 

displacement of, 566 

enlargement of, 566 

examination of, 563 

inspection of, 564 

pain in region of, 566 

palpation of, 564 

percussion of, 567 

point, 566 

pulsations of, 466 

puncture of, exploratory, 65 

tenderness in region of, 566 
Splenic flexure, clinical anatomy, 546 

friction-sound, 569 

systolic bruit, 569 
Splenization, pulmonary, 191 
Splenotosis, 567 

Sputum in croupous pneumonia, 210 
Stenosis aortic, 469. See also Aortic 
stenosis. 

funnel-shaped, mitral, 451 

mitral, 45 1 . See also Mitral stenosis. 

of bronchi, 187 

of upper air-passages as cause of 
dyspnea, 104 

pulmonary, 479 

clinical pathology, 479 
congenital, 485 
diagnosis of, 481 



Stenosis, pulmonary, physical signs, 480 
pulse in, 480 
relative, 480 

soft-valve, mitral, 453 

subaortic, 471 

tricuspid, 477. See also Tricuspid 
stenosis. 
Sternal dulness, 147 

line, 76 

pain, 119 

region, 79 

thrill over, 336 
Sternomastoid breathing, 97 
Sternum as landmark of thorax, 73 

enlargement of veins about, 107 
Stertorous respiration, 101 
Stethoscope, Arnold's, 26 

binaural, 24 

Bowies', 24 

choice, 23 

differential, 26 

double, 24 

Hawksley's, 26 

monaural, 24 

Sansom's, 25 

single, 24 
Stiller's sign, 539 
Stokes-Adams' bradycardia, 376 

heart-block, 375 
Stomach, auscultation of, 543 

auscultatory percussion of, 542 

body of, clinical anatomy, 532 

canal of, clinical anatomy, 532 

cancer of, pain in, 538 
x-ray examination in, 537 

clinical anatomy, 531 

contents, effervescence of, 543 

deglutition murmur of, 543 

examination of, 531 

fundus of, clinical anatomy, 532 

greater curvature of, clinical anat- 
omy, 533 

gurgling in, 543 

hour-glass, 535 

incisura angularis of, clinical anat- 
omy, 533 

inspection of, 533 

lesser curvature of, clinical anatomy, 

mechanical inflation, 534 

pain in, 538 

palpation of, 537 

percussion of, 541 

perforation of, metallic rub in, 543 

peristalsis of, 524 

sounds, 515 

stroke auscultation of, 543 

succussion sounds of, 539 



INDEX 



599 



Stomach, transillumination of, 537 

tumors of, pain in, 538 

tympany of, decrease, 543 
increase, 543 

ulcer of, pain of, 538 

x-ray examination in, 537 

vestibule of, clinical anatomy, 532 

x-ray examination, 536 
Stomach-tube, use of 539 
Stone-cutter's phthisis, 259 
Striae vasculares in chronic ulcerative 

phthisis, 232 
Stridor serraticus, 102 
Stridulous respiration, 101 
String galvanometer, Lewis' diagram 

of, 45 
Stripe pneumonia, 205 
Stroke auscultation, 16 

of stomach, 543 
Subaortic stenosis, 471 
Subclavian artery, aneurism of, 502 
pressure of cervical rib on, 504 
Subcostal angle, 75 

respiratory alterations of, 96 
Subcrepitant rales, 168 
Subcrepitations, atelectatic, 169 
Subcutaneous nodules of abdomen, 526 

tissue of abdomen, 525 
Submaxillary glands, enlargement, 112 
Subphrenic pyopneumothorax, 301 
Subpleural crepitation, 172 
Succussio Hippocratis in pneumo- 
thorax, 299 
succussion fremitus, 137 

sounds, 173 

Hippocratic, 174 
of stomach, 539 
pericardial, 400 
Suffocating gases, effects of, 193 
Suffocative catarrh, 197, 200 

edema of lungs, 193 
Suffusion, venous, of neck, 131 
Sulcus, Harrison's, 85 
Suppurative mediastinal lymphaden- 
itis, 306 

mediastinitis, 304 
Supracardiac vascular area, clinical 

anatomy, 318 
Supraclavicular region, 79 
Suprascapular region, 79 
Symphysis pleurae, 290 

pubis, 508 
Syndrome, effort, 403, 406, 461 
sinus arhythmia in, 407 

Spens', 376 

Stokes-Adams', 376 
Syphilis, pulmonary, 244 
acquired, 244 



Syphilis, pulmonary, clinical pathology, 
244 
congenital, 245 
diagnosis, 245 
physical signs, 245 
Syphilitic pneumonia, 244 
Systole, auricular, 321 

ventricular, 322 
Systolic bruit over spleen, 569 
epigastric throbbing, 332 
murmurs, 383 
aortic, 392 
apical, 386 
arterial, 400 
mitral, 391 
pulmonic, 386, 395 
tricuspid, 386, 393 
plateau, 42, 328 
souffle over gall-bladder, 562 
venous pulse, 356 » 



Tachycardia, 341 

auricular, 342 

paroxysmal, 343 
Tactile friction of abdomen, 528 
Tawara's node, 321 
Test, Calmette's, 70 

epinephrin, 404 

exercise, 403 

Gairdner's, 154 

Koch's tuberculin, 68 

pulse pressure, 404 

von Pirquet's, 69 
Thoracic aorta, aneurism of, 488. See 
also Aneurism- of thoracic aorta. 

glands, lateral, enlargement of, 116 

index, Fourmentin's, 72 

respiration, 95 

vertebra, twelfth line of, 79 
Thoracometry, 29 
Thorax, alar, 80 

anterior, percussion of, 138 

asymmetry of, 88 

barrel-, 80, 81 

boat-shaped, 88 

clavicles as landmarks of, 73 

clinical anatomy, 72 

depressions of, local, 92 

edema of, 108 

emphysematous, 80 

en bateau, 88 

en gouttiere, 88 

examination of, 72 

expansion of, alterations in degree, 97 
deficiency in, 97 
Bryson's sign, 98 
circumscribed, 98 



6oo 



INDEX 



Thorax, expansion of, increase in, 98 
unsymmetric, 98 
wavy and uneven, 98 

expiratory form, 80 

flat, 86 

fusiform, 87 

glandular enlargements, in 

gutter-, 88 

inflated, 80 

inspiratory form, 82 

intercostal spaces as landmarks of, 74 

lateral regions, percussion of, 138 
wall, pain in, 121 

lower, enlargement of veins of, 108 

mensuration of, 29 

movements of, mechanical restric- 
tion as cause of dyspnea, 105 

nipple as landmark of, 75 

normal landmarks, 73 

of atrophic emphysema, 82 

of progressive muscular atrophy, 88 

pain in, 119 

paralytic, 80 

pathologic types, 79 

phthisical, 80 

posterior wall, pain in, 121 

prominences of, circumscribed, 91 

pterygoid, 80 

rachitic, 8s 

respiratory movements, 94. See also 
Respiration. 

ribs as landmarks of, 74, 75 

scars of, 123 

sternum as landmark, 73 

topographic lines and areas, 76 

unilateral bulging, 88 
contraction, 90 

upper, ramification of small venules 
over, 107 

venous enlargement and tortuosity 
over, 106 

vertical measurement, 72 
Threshold percussion, Goldscheider's 

method, 14 
Thrill, 335 

abdominal, 528 

at apex of heart, 335 

at base of heart, 335 

at intercostal spaces, 335 

hydatid, 528 

over sternal region, 336 

over xiphoid region, 336 

palpable, in epigastrium, 528 
Thymus gland, movable dulness of, 504 
Thyroid gland, enlargement, 118 
Tinkling, metallic, 174 
Tortuous and enlarged veins over 

abdomen, 526 



Toxemic dyspnea, 103 
Toxic pneumonia, 214 
Trachea, clinical anatomy, 128 
rales, 166 

tone, Williams', 153 
tugging, 336 
Tracheobronchitic stage of gassing, 194 
Tracheobronchitis, acute, 175 
Transudate in pleural fluid, 53 
Traube's plugs in fetid bronchitis, 179 
semilunar space, 542 
sign in aortic regurgitation, 469 
space, dulness of normal tympany 
in, 147 
Traumatic pneumonia, 216 
Triangle, sacral, 509 
Trichertbrust, 85 
Tricuspid area, 364 
murmurs, 393 
presystolic, 393 
systolic,_ 386, 393 
regurgitation, 474 

clinical pathology, 474 
diagnosis, 477 
organic, 474 
physical signs, 475 
pulse in, 476 
relative, 475 
stenosis, 477 

clinical pathology, 477 
diagnosis, 479 
physical signs, 478 
pulse in, 478 
valve, clinical anatomy, 318 
True aneurism of thoracic aorta, 490 
Trypanosoma gambiense in cerebro- 
spinal fluid, 65 
Tubercle friction, 515 

in tuberculous peritonitis, 528 
Tuberculin reaction, 68 
test, Calmette's, 70 
Koch's, 68 
von Pirquet's, 69 
Tuberculofibrosis of lungs, 241 
Tuberculosis, chronic ulcerative, Ras- 
mussen's aneurism in, 228 
hilus, 229, 240 
of bronchial glands, 306 
Tugging, tracheal, 336 
Tumors of mediastinum, 309 
clinical pathology, 309 
diagnosis, 313 
physical signs, 310 
of pleura, 302 
of stomach, pain in, 538 
pulmonary, 267 
Tuning-fork auscultation, 28 
Turrettini's sign, 409 



INDEX 



60 1 



Tussive fremitus, 137 
Tympanic percussion-sounds, 13, 19 
Tympanites, pulmonary, 147-149 
Tympany, bell, 154 

from parabronchial consolidations, 

154 
gastric, decrease of, 543 

increase of, 543 
in bronchiectatic cavities, 149 
in pneumothorax, 150 
in pulmonary cavities, 149 
pulmonary, 147 

acute, 149 
Typhoid pneumonia, 214 



Ulcer, gastric, pain of ,538 

#-ray examination in, 537 
Ulcerative endocarditis, 435 
phthisis, chronic, 226. See also 
Phthisis j chronic ulcerative. 
Ulceres du poumon, 262 
Umbilical changes, 526 
notch, 552 
region, 511 
pain in, 530 
Umbilicus, 509 
Uremic dyspnea, 103 
U. S. Army exercise test for functional 
capacity of heart, 403 



Vagus lag, 403 
Valves, aortic, 318 

areas of, 318 
of heart, 364 

beaded excrescences of, 435 

ileocecal, 545 

mitral, 318 

of heart, 318 

polypous lesions of, 435 

pulmonic, 318 

tricuspid, 318 

verrucose excrescences of, 435 

villous lesions of, 435 
Valvular disease, chronic, 439 
Valvulitis, 433 
Varicose aneurism, 491 
Varix, aneurismal, 490 
Vascular dulness, area of, 360 

murmurs, 400 
Veiled puff, Laennec's, 159 
Veines fluides, 382 
Veins, cervical, respiratory, turgescence, 

131 

engorgement of, 334 

enlarged and tortuous, over abdo- 
men, 526 



Veins, enlargement of, about sternum, 
107 

of costal arch, 108 

of lower thorax, 108 

of upper arm, 107 

over thorax, 106 
fluid, 382 

innominate, clinical anatomy, 319 
jugular, diastolic collapse, 331 

engorgement of, 334 

pulsation of, 330 
mammary, enlarged, 107 
ramification of, over upper chest, 107 
tortuosity of, over thorax, 106 
Vena cava, inferior, clinical anatomy, 

509 
superior, aneurism of, 502 
clinical anatomy, 319 
Venous blood-pressure, instrumental 
estimation, 37 
Oliver's method of estimating, 37 
bruit, hepatic, 562 
engorgement, S33 
flow, direction of, 107 
hum, 402 
pulse, 354 
auricular, 355 
in aortic regurgitation, 465 
penetrating, 357 
physiologic, 42 
ventricular, 356 
sphygmogram, 42 
suffusion of neck, 131 
Ventricular diastole, 322 
extrasystoles, 373 
fibrillation, 378 
systole, 322 
Vermiform appendix, clinical anatomy, 

545 
Verneuil's pseudohpoma, 92 
Verrucose excrescences of valves, 435 
Vertebra, twelfth thoracic, line of, 

79 

Vertebral reflexes, 22 

Vesicular emphysema, 241. See also 
Emphysema, pulmonary. 
rales, 166 
resonance, 166. See also Resonance, 

pulmonary. 
respiration, 156 

Vesiculocavernous respiration, 158 

Vesiculotympanitic resonance, 148 

Vesiculotympany in hypertrophic em- 
physema of lungs, 251 

Vicarious emphysema of lungs, 253 

Villous lesions of valves, 435 

Viscera, abdominal, examination of, 
507 



^> 






602 



INDEX 



Viscera, abdominal, topographic lines 

and areas, 510 
Visceral paracentesis, 65 

pleura, 128 
Vocal fremitus, 134 

resonance, 163 
Voice fremitus, influence of decubitus 

on, 135 
Voillemier's point, 531 
von Pirquet's tuberculin test, 69 



Waist, wasp, 88 

Wandering pneumonia, 205 

Wassermann reaction in cerebrospinal 
fluid, 65 

Water-hammer pulse in aortic regur- 
gitation, 466 

Water- whistle noise, 169 
in pneumothorax, 299 

Wheeze, asthmatoid, 102 

Whispering pectoriloquy, 163 

White hepatization of lungs, 244 



White pneumonia, 244 

of fetus, 245 
Williams' sign in phthisis, 233 

tracheal tone, 152 
Winged scapulae, 80 
Winter cough, 178 
.Wintrich's interrupted change of note 

152 
sign, 151 
Woillez's disease, 190 

Xiphisternal crunching, 366 

joint, 73 
Xiphoid crepitation, 528 

region, thrill over, 336 
X-rays. See Rontgen rays. 

Yperite, effects of, 200 



Zagoumenny's rule, 54 
Zones, spinal percussion, 21 



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